scholarly journals Coats’ Disease-Related Macular Edema Treated with Combined Aflibercept and Laser Photocoagulation

2017 ◽  
Vol 2017 ◽  
pp. 1-3 ◽  
Author(s):  
Wen-Shi Shieh ◽  
Gaurav K. Shah ◽  
Kevin J. Blinder

Purpose. To describe the clinical response of refractory macular edema associated with Coats’ disease following treatment with aflibercept and laser photocoagulation. Methods. Case report. Results. A 17-year-old female presented with decreased vision of the left eye. Ophthalmic exam demonstrated intraretinal hemorrhages and exudation with associated edema centrally. Angiographic evaluation revealed central leaking microaneurysms and peripheral capillary dropout. These findings and a systemic work-up that yielded an incidental Factor V Leiden mutation lead to a diagnosis of Coats’ disease. Initial treatment consisted of laser photocoagulation and intravitreal bevacizumab but with poor response. Switching to intravitreal aflibercept resulted in resolution of the refractory macular edema and improvement of visual acuity to 20/25 in the left eye. Conclusion. We describe a case of refractory macular edema which responded more favorably to intravitreal aflibercept compared with bevacizumab when combined with laser photocoagulation in a patient with Coats’ disease.

2019 ◽  
Vol 3 (6) ◽  
pp. 480-484
Author(s):  
Cristy A. Ku ◽  
Gareth M. Lema

Purpose: This case is the first to our knowledge that demonstrates the efficacy of intravitreal aflibercept in bevacizumab-resistant, laser-naive macular edema (ME) in adult-onset Coats disease. Methods: A retrospective case report is presented. Results: A 74-year-old woman presented with central visual distortion in her right eye. Imaging and exam were consistent with adult-onset Coats disease with unilateral telangiectatic vessels, numerous macroaneurysms, and peripheral capillary dropout. There were also ME, lipid exudate, and localized hemorrhage. ME failed to respond to 4 intravitreal injections of bevacizumab but dramatically improved following initiation of aflibercept, with patient deferral of laser photocoagulation. Conclusions: To our knowledge, this is the first reported case of aflibercept as the sole treatment of bevacizumab-resistant ME in adult-onset Coats disease. Given the localized macular involvement more common to adult-onset Coats disease, antivascular endothelial growth factor (anti-VEGF) therapy may be sufficient, compared with classic childhood Coats disease, in which anti-VEGF therapy serves as an adjunct to laser photocoagulation or cryotherapy.


VASA ◽  
2015 ◽  
Vol 44 (4) ◽  
pp. 313-323 ◽  
Author(s):  
Lea Weingarz ◽  
Marc Schindewolf ◽  
Jan Schwonberg ◽  
Carola Hecking ◽  
Zsuzsanna Wolf ◽  
...  

Abstract. Background: Whether screening for thrombophilia is useful for patients after a first episode of venous thromboembolism (VTE) is a controversial issue. However, the impact of thrombophilia on the risk of recurrence may vary depending on the patient’s age at the time of the first VTE. Patients and methods: Of 1221 VTE patients (42 % males) registered in the MAISTHRO (MAin-ISar-THROmbosis) registry, 261 experienced VTE recurrence during a 5-year follow-up after the discontinuation of anticoagulant therapy. Results: Thrombophilia was more common among patients with VTE recurrence than those without (58.6 % vs. 50.3 %; p = 0.017). Stratifying patients by the age at the time of their initial VTE, Cox proportional hazards analyses adjusted for age, sex and the presence or absence of established risk factors revealed a heterozygous prothrombin (PT) G20210A mutation (hazard ratio (HR) 2.65; 95 %-confidence interval (CI) 1.71 - 4.12; p < 0.001), homozygosity/double heterozygosity for the factor V Leiden and/or PT mutation (HR 2.35; 95 %-CI 1.09 - 5.07, p = 0.030), and an antithrombin deficiency (HR 2.12; 95 %-CI 1.12 - 4.10; p = 0.021) to predict recurrent VTE in patients aged 40 years or older, whereas lupus anticoagulants (HR 3.05; 95%-CI 1.40 - 6.66; p = 0.005) increased the risk of recurrence in younger patients. Subgroup analyses revealed an increased risk of recurrence for a heterozygous factor V Leiden mutation only in young females without hormonal treatment whereas the predictive value of a heterozygous PT mutation was restricted to males over the age of 40 years. Conclusions: Our data do not support a preference of younger patients for thrombophilia testing after a first venous thromboembolic event.


1998 ◽  
Vol 80 (08) ◽  
pp. 344-345 ◽  
Author(s):  
Pasra Arnutti ◽  
Motofumi Hiyoshi ◽  
Wichai Prayoonwiwat ◽  
Oytip Nathalang ◽  
Chamaiporn Suwanasophon ◽  
...  

1995 ◽  
Vol 74 (05) ◽  
pp. 1255-1258 ◽  
Author(s):  
Arnaldo A Arbini ◽  
Pier Mannuccio Mannucci ◽  
Kenneth A Bauer

SummaryPatients with hemophilia A and B and factor levels less than 1 percent of normal bleed frequently with an average number of spontaneous bleeding episodes of 20–30 or more. However there are patients with equally low levels of factor VIII or factor IX who bleed once or twice per year or not at all. To examine whether the presence of a hereditary defect predisposing to hypercoagulability might play a role in amelio rating the hemorrhagic tendency in these so-called “mild severe” hemophiliacs, we determined the prevalence of prothrombotic defects in 17 patients with hemophilia A and four patients with hemophilia B selected from 295 and 76 individuals with these disorders, respectively, followed at a large Italian hemophilia center. We tested for the presence of the Factor V Leiden mutation by PCR-amplifying a fragment of the factor V gene which contains the mutation site and then digesting the product with the restriction enzyme Mnll. None of the patients with hemophilia A and only one patient with hemophilia B was heterozygous for Factor V Leiden. None of the 21 patients had hereditary deficiencies of antithrombin III, protein C, or protein S. Our results indicate that the milder bleeding diathesis that is occasionally seen among Italian hemophiliacs with factor levels that are less than 1 percent cannot be explained by the concomitant expression of a known prothrombotic defect.


1996 ◽  
Vol 75 (03) ◽  
pp. 520-521 ◽  
Author(s):  
D C Rees ◽  
M Cox ◽  
J B Clegg

1996 ◽  
Vol 75 (03) ◽  
pp. 422-426 ◽  
Author(s):  
Paolo Simioni ◽  
Alberta Scudeller ◽  
Paolo Radossi ◽  
Sabrina Gavasso ◽  
Bruno Girolami ◽  
...  

SummaryTwo unrelated patients belonging to two Italian kindreds with a history of thrombotic manifestations were found to have a double heterozygous defect of factor V (F. V), namely type I quantitative F. V defect and F. V Leiden mutation. Although DNA analysis confirmed the presence of a heterozygous F. V Leiden mutation, the measurement of the responsiveness of patients plasma to addition of activated protein C (APC) gave results similar to those found in homozygous defects. It has been recently reported in a preliminary form that the coinheritance of heterozygous F. V Leiden mutation and type I quantitative F. V deficiency in three individuals belonging to the same family resulted in the so-called pseudo homozygous APC resistance with APC sensitivity ratio (APC-SR) typical of homozygous F. V Leiden mutation. In this study we report two new cases of pseudo homozygous APC resistance. Both patients experienced thrombotic manifestations. It is likely that the absence of normal F. V, instead of protecting from thrombotic risk due to heterozygous F. V Leiden mutation, increased the predisposition to thrombosis since the patients became, in fact, pseudo-homozygotes for APC resistance. DNA-analysis is the only way to genotype a patient and is strongly recommended to confirm a diagnosis of homozygous F. V Leiden mutation also in patients with the lowest values of APC-SR. It is to be hoped that no patient gets a diagnosis of homozygous F. V Leiden mutation based on the APC-resi-stance test, especially when the basal clotting tests, i.e., PT and aPTT; are borderline or slightly prolonged.


1996 ◽  
Vol 76 (02) ◽  
pp. 275-277 ◽  
Author(s):  
Sylvie Hollemaert ◽  
Jean-Claude Wautrecht ◽  
Paul Capel ◽  
Marc J Abramowicz ◽  
Yvon Englert ◽  
...  

1997 ◽  
Vol 78 (04) ◽  
pp. 1297-1298 ◽  
Author(s):  
Marie-Hélène Denninger ◽  
Dominique Helley ◽  
Dominique Valla ◽  
Marie-Claude Guillin

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