Zur Klinik und Anatomie der gefäßähnlichen Streifen im Augenhintergrund (Part 1 of 2)

Bock, Jang Jun

doi:10.1159/000299514

Cited by 11 publications

(12 citation statements)

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“…This is now the accepted view, and has been confirmed histologically by Bock (1938), Hagedoorn (1939, Klien (1947), Verhoeff (1948), and others. All their histological studies were made on patients with elastorrhexis; the common ocular findings were:…”

Section: Histologymentioning

confidence: 57%

Angioid streaks and elastorrhexis.

Percival¹

1968

British Journal of Ophthalmology

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Section: Histologymentioning

confidence: 57%

Angioid streaks and elastorrhexis.

Percival¹

1968

British Journal of Ophthalmology

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“…It took more than two further decades before Kofler, based on meticulous clinical observations, eventually suggested that angioid streaks are due to breaks in BM (Kofler, 1917). His observations were later supported by histological studies (Böck, 1938; Hagedoorn, 1939; Verhoeff, 1948; McWilliam, 1951; Jensen, 1977; Dreyer and Green, 1978) and were more recently confirmed by in vivo imaging (Charbel Issa et al, 2009). In 1941, Scholz provided an excellent thorough review of the early literature on angioid streaks, analyzing a total of 188 reported cases (Scholz, 1941).…”

Section: Historical Notes and Terminologymentioning

confidence: 85%

“…Several authors noted a patchy transition zone towards the rather normal appearing peripheral BM anterior to the equator (Böck, 1938; Hagedoorn, 1939; Klien, 1947; Verhoeff, 1948; Jensen, 1977). This transition zone may be the histopathological correlate for peau d’orange, although no direct evidence has been provided for this interpretation.…”

Section: Histologymentioning

confidence: 99%

“…The histopathological correlate for angioid streaks– breaks in the calcified BM – has been documented in donor eyes of patients with PXE (Böck, 1938; Hagedoorn, 1939; Verhoeff, 1948; Gass, 1967; Jensen, 1977; Dreyer and Green, 1978; Mansour, 1998), Paget’s disease (Gass and Clarkson, 1973), sickle cell disease (Jampol et al, 1987), and of patients without defined underlying disease (Klien, 1947; McWilliam, 1951; Domke and Tost, 1964; Gass, 1967; Dreyer and Green, 1978). Small breaks may remain without morphological changes in the overlying layers of the RPE and retina or of the underlying choriocapillaris.…”

Section: Histologymentioning

confidence: 99%

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An update on the ocular phenotype in patients with pseudoxanthoma elasticum

Gliem¹,

Zaeytijd²,

Finger³

et al. 2013

Front. Genet.

121

206

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Pseudoxanthoma elasticum (PXE) is an inherited multi-system disorder characterized by ectopic mineralization and fragmentation of elastic fibers in the skin, the elastic laminae of blood vessels and Bruch’s membrane in the eye. Biallelic mutations in the ATP-binding cassette (ABC) transporter gene ABCC6 on chromosome 16 are responsible for the disease. The pathophysiology is incompletely understood. However, there is consent that a metabolic alteration leads to dysfunction in extracellular calcium homeostasis and subsequent calcification of connective tissues rich in elastic fibers. This review summarizes and aims at explaining the variety of phenotypic ocular findings in patients with PXE. Specialized imaging techniques including white light fundus photography, blue light autofluorescence, near-infrared confocal reflectance imaging, high resolution optical coherence tomography, fluorescein and indocyanine green (ICG) angiography have revealed characteristic lesions at the ocular fundus of PXE patients. These include the classic signs of angioid streaks, peau d’orange, comet lesions, and choroidal neovascularizations (CNVs), but also the more recently recognized features such as chorioretinal atrophy, subretinal fluid independent from CNV, pattern dystrophy-like changes, debris accumulation under the retinal pigment epithelium, reticular drusen and a decreased fluorescence on late phase ICG angiography.

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“…Not until 1917 did Kofler3 correctly determine that angioid streaks represented changes at the level of Bruch’s membrane. Clinical examination with subsequent histopathological findings by Bock4 in 1938 in two patients with pseudoxanthoma elasticum confirmed that the underlying abnormality was not vascular in nature but rather a structural alteration in Bruch’s membrane. A few years later similar histopathological results were found in patients suffering pseudoxanthoma elasticum, Paget’s disease, but also from systemic diseases 5.…”

Section: Introductionmentioning

confidence: 84%

Angioid streaks, clinical course, complications, and current therapeutic management

Georgalas¹

2008

TCRM

101

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Angioid streaks are visible irregular crack-like dehiscences in Bruch's membrane that are associated with atrophic degeneration of the overlying retinal pigmented epithelium. Angioid streaks may be associated with pseudoxanthoma elasticum, Paget's disease, sickle-cell anemia, acromegaly, Ehlers-Danlos syndrome, and diabetes mellitus, but also appear in patients without any systemic disease. Patients with angioid streaks are generally asymptomatic, unless the lesions extend towards the foveola or develop complications such as traumatic Bruch's membrane rupture or macular choroidal neovascularization (CNV). The visual prognosis in patients with CNV secondary to angioid streaks if untreated, is poor and most treatment modalities, until recently, have failed to limit the devastating impact of CNV in central vision. However, it is likely that treatment with antivascular endothelial growth factor, especially in treatment-naive eyes to yield favorable results in the future and this has to be investigated in future studies.

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Zur Klinik und Anatomie der gefäßähnlichen Streifen im Augenhintergrund (Part 1 of 2)

Cited by 11 publications

References 0 publications

Angioid streaks and elastorrhexis.

Angioid streaks and elastorrhexis.

An update on the ocular phenotype in patients with pseudoxanthoma elasticum

Angioid streaks, clinical course, complications, and current therapeutic management

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