Primary Telangiectasia of Childhood

Abrahamian, Lori M.; Rothe, Marti Jill; Grant‐Kels, Jane M.

doi:10.1111/j.1365-4362.1992.tb03943.x

Cited by 16 publications

(20 citation statements)

References 40 publications

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“…Apart from the family history, telangiectases are required for the diagnosis of HBT, but in some patients the diagnosis may be missed because the few telangiectases may be atypically located and tend to fade with age [6]. VCP can be a simple, noninvasive method for disclosing additional microscopic abnormalities, since giant loops at the nailfold in these patients can be regarded as ‘microscopic telangiectases’.…”

Section: Discussionmentioning

confidence: 99%

Hereditary Benign Telangiectasia: Videocapillaroscopic Findings

et al. 2003

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Section: Discussionmentioning

confidence: 99%

Hereditary Benign Telangiectasia: Videocapillaroscopic Findings

et al. 2003

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“…Such patients, however, would have a different family history, because the lesions fade with age. 17 The diagnosis of HHT may be difficult because of few or atypical telangiectases. This is the case particularly in young patients, because telangiectases usually start to appear at an adult age.…”

Section: Commentmentioning

confidence: 99%

Value of Capillary Microscopy in the Diagnosis of Hereditary Hemorrhagic Telangiectasia

Mager¹,

Westermann²

2000

Arch Dermatol

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“…It may be secondary to vari- ous conditions, or a primary idiopathic disorder of an unknown cause (Table 1). [2][3][4][5][6][7][8] The common telangiectases represent abnormalities in the organization and ultrastructure of the microvasculature, but not neovascularization or random anastomoses. 1 Macular telangiectases are caused by dilatation of post-capillary venules (PCV) of the upper horizontal plexus.…”

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confidence: 99%

Cutaneous collagenous vasculopathy with generalized telangiectasia: an immunohistochemical and ultrastructural study

2000

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We report a 54-year-old male, with a 5-year history of spreading asymptomatic generalized cutaneous telangiectases. The patient had no mucosal or nail involvement, no positive family history and no clinical evidence of systemic disease or bleeding diathesis. Histologically, the superficial small dermal blood vessels were dilated and showed thickened walls with hyaline perivascular material, staining as collagen. The vessel walls were PAS and colloidal iron stain positive, and immuno-histochemically lacked actin staining. Collagen IV, fibronectin and laminin antibodies showed the material deposited around the basement membrane zone. Ultrastructurally, the vessels were post-capillary venules (PCV) and showed marked collagen deposition around the basal lamina. There were many abnormally banded widely spaced fibres with 100-150 nm periodicity (Luse bodies), in addition to regular banded collagen. Pericytes were sparse and lacked intracytoplasmic filaments, and few veil or fibroblastic cells were seen embedded within the collagen. We believe this is a form of cutaneous microangiopathy not previously described, with distinct morphology and unique ultrastructural features. It may be due to a genetic defect with erroneous production of disorganized collagen in the cutaneous microvasculature. Dermatologists and Dermatopathologists should be aware of this unusual cutaneous vasculopathy.

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Primary Telangiectasia of Childhood

Cited by 16 publications

References 40 publications

Hereditary Benign Telangiectasia: Videocapillaroscopic Findings

Hereditary Benign Telangiectasia: Videocapillaroscopic Findings

Value of Capillary Microscopy in the Diagnosis of Hereditary Hemorrhagic Telangiectasia

Cutaneous collagenous vasculopathy with generalized telangiectasia: an immunohistochemical and ultrastructural study

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