Angioendotheliomatosis

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 555 Experts worldwide ranked by ideXlab platform

Elena Levtchenko - One of the best experts on this subject based on the ideXlab platform.

  • Increased human dermal microvascular endothelial cell survival induced by cysteamine
    Journal of Inherited Metabolic Disease, 2013
    Co-Authors: M. Besouw, I. Bongaers, Leo A. J. Kluijtmans, M. Dewerchin, L. Heuvel, R. Eijsden, Elena Levtchenko
    Abstract:

    Background Cystinosis is an autosomal recessive disease caused by intralysosomal cystine accumulation, treated with cysteamine. Recently, new adverse effects of cysteamine were reported. Skin biopsies showed microvascular proliferation (Angioendotheliomatosis). To examine the mechanism of Angioendotheliomatosis associated with cysteamine toxicity, we examined the effect of cysteamine on human dermal microvascular endothelial cells (HDMVEC). Methods After cysteamine exposure (range 0–3.0 mM) during 24 h, cell viability was measured using water soluble tetrazolium salt-1 (WST-1) in both control HDMVEC and fibroblasts. Cell proliferation and apoptosis rate were measured in HDMVEC by bromodeoxyuridine (BrdU) incorporation and caspase 3 and caspase 7 activity, respectively. Intracellular glutathione (GSH) was measured in HDMVEC after cysteamine exposure of 0, 0.1 or 1.0 mM. Medium and cysteamine were refreshed every 6 h to mimic the in vivo situation. Next, cell viability in HDMVEC was measured after 24 h of GSH exposure (range 0–10.0 mM). Results HDMVEC viability and proliferation increased after cysteamine exposure 0.03–3.0 mM ( p  

  • Increased human dermal microvascular endothelial cell survival induced by cysteamine
    Journal of inherited metabolic disease, 2013
    Co-Authors: M. Besouw, L.p.w.j. Van Den Heuvel, R. Van Eijsden, I. Bongaers, Leo A. J. Kluijtmans, M. Dewerchin, Elena Levtchenko
    Abstract:

    Background Cystinosis is an autosomal recessive disease caused by intralysosomal cystine accumulation, treated with cysteamine. Recently, new adverse effects of cysteamine were reported. Skin biopsies showed microvascular proliferation (Angioendotheliomatosis). To examine the mechanism of Angioendotheliomatosis associated with cysteamine toxicity, we examined the effect of cysteamine on human dermal microvascular endothelial cells (HDMVEC).

M. Besouw - One of the best experts on this subject based on the ideXlab platform.

  • Increased human dermal microvascular endothelial cell survival induced by cysteamine
    Journal of Inherited Metabolic Disease, 2013
    Co-Authors: M. Besouw, I. Bongaers, Leo A. J. Kluijtmans, M. Dewerchin, L. Heuvel, R. Eijsden, Elena Levtchenko
    Abstract:

    Background Cystinosis is an autosomal recessive disease caused by intralysosomal cystine accumulation, treated with cysteamine. Recently, new adverse effects of cysteamine were reported. Skin biopsies showed microvascular proliferation (Angioendotheliomatosis). To examine the mechanism of Angioendotheliomatosis associated with cysteamine toxicity, we examined the effect of cysteamine on human dermal microvascular endothelial cells (HDMVEC). Methods After cysteamine exposure (range 0–3.0 mM) during 24 h, cell viability was measured using water soluble tetrazolium salt-1 (WST-1) in both control HDMVEC and fibroblasts. Cell proliferation and apoptosis rate were measured in HDMVEC by bromodeoxyuridine (BrdU) incorporation and caspase 3 and caspase 7 activity, respectively. Intracellular glutathione (GSH) was measured in HDMVEC after cysteamine exposure of 0, 0.1 or 1.0 mM. Medium and cysteamine were refreshed every 6 h to mimic the in vivo situation. Next, cell viability in HDMVEC was measured after 24 h of GSH exposure (range 0–10.0 mM). Results HDMVEC viability and proliferation increased after cysteamine exposure 0.03–3.0 mM ( p  

  • Increased human dermal microvascular endothelial cell survival induced by cysteamine
    Journal of inherited metabolic disease, 2013
    Co-Authors: M. Besouw, L.p.w.j. Van Den Heuvel, R. Van Eijsden, I. Bongaers, Leo A. J. Kluijtmans, M. Dewerchin, Elena Levtchenko
    Abstract:

    Background Cystinosis is an autosomal recessive disease caused by intralysosomal cystine accumulation, treated with cysteamine. Recently, new adverse effects of cysteamine were reported. Skin biopsies showed microvascular proliferation (Angioendotheliomatosis). To examine the mechanism of Angioendotheliomatosis associated with cysteamine toxicity, we examined the effect of cysteamine on human dermal microvascular endothelial cells (HDMVEC).

Eduardo Fonseca - One of the best experts on this subject based on the ideXlab platform.

  • Reactive Angioendotheliomatosis associated with myelodysplastic syndrome.
    Acta dermato-venereologica, 2005
    Co-Authors: Jesús Del Pozo, W. Martínez, Felipe Sacristán, J. Rodríguez‐lozano, Eduardo Fonseca
    Abstract:

    Sir, Although Gottron & Nikolowsky (1) probably reported the first case of Angioendotheliomatosis in 1958, this term was proposed in 1963 by Tappeiner & Pfleger (2), who described a proliferation of endothelial cells within the lumen of dermal vessels with secondary necrosis and infarction of the skin. To our knowledge, only 39 cases of reactive Angioendotheliomatosis have been reported in the literature, usually as isolated cases, except the series of 15 cases published by McMenamin & Flether (3). The association of reactive Angioendotheliomatosis with systemic diseases is common, but some exceptional cases have been described without any association (4). Several factors may play an important role in this process, including angiogenic circulant factors (5) such as VEGF, procoagulant factors and localized hypoxia that produces oxidative stress with release of free radicals. We report here a case of reactive Angioendotheliomatosis with crusted-necrotic ear lesions after cold exposure. The patient also had a myelodysplastic syndrome.

K. Nagashima - One of the best experts on this subject based on the ideXlab platform.

  • Two cases of neoplastic Angioendotheliomatosis presenting with myelopathy.
    Neurology, 1991
    Co-Authors: K. Hamada, Takeshi Hamada, M. Satoh, Kunio Tashiro, I. Katoh, Mutsuo Naganuma, Shima K, Akihiko Ogata, K. Nagashima
    Abstract:

    We describe two patients with autopsy-proven neoplastic Angioendotheliomatosis (NAE) presenting only as a transverse myelopathy for 10 to 12 months, followed by disseminated intracranial manifestations. Postmortem examination disclosed a vasculocentric distribution of neoplastic cells in various organs that stained positively with B-lymphocyte-specific monoclonal antibody. These cases were unusual because they manifested as an isolated myelopathy for many months.

Hector Battifora - One of the best experts on this subject based on the ideXlab platform.

  • Intravascularly disseminated angiosarcoma: true neoplastic Angioendotheliomatosis? Report of two cases.
    The American journal of surgical pathology, 1997
    Co-Authors: Bryan T.-y. Lin, Lawrence M. Weiss, Hector Battifora
    Abstract:

    Although vascular invasion is common in many malignant tumors, disseminated intravascular anaplastic neoplasms with occult primary tumor are rare occurrences. Intravascular malignant lymphoma, also called angiotropic lymphoma, is a rare variant of large cell lymphoma predominantly involving vessels in multiple organs, and usually without significant nodal involvement. Although initially misinterpreted as an endothelial neoplasm-Angioendotheliomatosis-immunohistochemical studies subsequently proved it to represent a peculiar form of malignant lymphoma. In this report, we describe two patients with extensive intravascular dissemination of angiosarcoma initially without clinically obvious primary tumor. These may be interpreted as examples of true Angioendotheliomatosis. In each case the immunohistochemical studies ruled out the most common intravascular malignant neoplasms. The diagnosis of intravascular angiosarcoma was confirmed by the immunoreactivity of the tumor cells to several markers of endothelial lineage in both cases. Thus, angiosarcoma may present with intravascular dissemination and occult primary tumor and closely resemble metastatic carcinoma, melanoma, or angiotropic lymphoma. Immunohistochemical studies are crucial in ruling out these possibilities and in confirming the endothelial origin of the neoplastic cells.