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  • 1
    Electronic Resource
    Electronic Resource
    Chemokine release from activated human dermal microvascular endothelial cells – implications for the pathophysiology of scleroderma? (2000)
    Springer
    Archives of dermatological research 292 (2000), S. 341-347 
    Details
    ISSN: 1432-069X
    Keywords: Key words RANTES ; MCP-1 ; Endothelial cells ; Chemotaxis ; Systemic sclerosis ; Silica ; Scleroderma ; Monocyte chemoattractant protein-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Long-term exposure to silica (SiO2) may induce silicosis as well as extrapulmonary diseases such as scleroderma. Infiltration of mononuclear cells and release of proinflammatory cytokines from these cells have been suggested to play a role in the development of inflammatory and immunological events typical of scleroderma as well as of silica-induced scleroderma. We showed that silica is able to directly activate cytokine expression in blood monocytes, collagenase expression in cultured dermal fibroblasts and ICAM-1 expression in human dermal microvascular endothelial cells. In the study reported here we found that silica and TNF· induce mRNA and protein of the chemokines RANTES and MCP-1 in endothelial cells. In addition, we demonstrated that culture supernatants of silica-treated endothelial cells are chemotactic for mononuclear cells from peripheral blood, suggesting that activation of endothelial cells may contribute to the chemotactic gradient necessary for extravasation of inflammatory blood cells into the surrounding tissue found in early scleroderma. However, a polyclonal anti-RANTES antibody failed to block chemotaxis suggesting that other proteins are involved in this phenomenon. We also studied the expression of RANTES in situ in the skin of systemic sclerosis patients and of healthy individuals. We found abundant RANTES mRNA expression in the skin of SSc patients, whereas in control skin no expression was found. From our data we conclude that RANTES and MCP-1 induction by silica may be an initiating event in inflammatory infiltration, whereas TNF·-mediated inflammation may propagate the disease more efficiently.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030000134
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  • 2
    Electronic Resource
    Electronic Resource
    Raynaud-Phänomen und Sklerodermie (1996)
    Springer
    Der Hautarzt 47 (1996), S. 336-340 
    Details
    ISSN: 1432-1173
    Keywords: Key words Raynaud-Phänomen ; Progressive Sklerodermie ; Gefäßtonus ; Neuropeptide ; Key words Raynaud phenomenon ; Systemic sclerosis ; Vascular tone ; Neuropeptides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The Raynaud phenomenon occurs in 90–100% of patients with systemic scleroderma. It is caused by dysregulation of the vascular tone between vasocontrictive and vasodilatory influences. Early damage to the vascular endothelium and the activation of platelets lead to the release of vasoactive substances. Structural and function impairment of the perivascular neural fibers contributes to the vasospasm. New vasodilatory treatment strategies, e.g. infusions with calcitonin gene-related peptides, could be useful in the control of vasospasm in the peripheral extremities as well as internal organs in systemic scleroderma.
    Notes: Zusammenfassung Das Raynaud-Phänomen kommt bei 90–100% der Patienten mit progressiver Sklerodermie vor. Es beruht auf einer Dysregulation des Gefäßtonus im Gleichgewicht von vasokonstriktorischen und vasodilatatorischen Einflüssen. Die frühzeitige Schädigung des Gefäßendothels und Aktivierung von Thrombozyten führen zur Freisetzung vasoaktiver Substanzen. Die strukturellen und funktionellen Veränderungen der perivaskulären Nervenfasern tragen zur Genese des Vasospasmus bei Sklerodermie bei. Neue Konzepte der gefäßerweiternden Therapie, wie z.B. Infusionen mit Calcitonin gen-related Peptiden könnten für die Verhinderung des Vasospasmus der peripheren Extremitäten und internen Organe bei der Sklerodermie nützlich sein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001050050427
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  • 3
    Electronic Resource
    Electronic Resource
    Stevens-Johnson-Syndrom mit Übergang in eine toxisch epidermale Nekrolyse nach Carbamazepin-Einnahme, Heroin- und Alkoholabusus (1999)
    Springer
    Der Hautarzt 50 (1999), S. 884-888 
    Details
    ISSN: 1432-1173
    Keywords: Schlüsselwörter Erythema exsudativum multiforme majus ; Stevens-Johnson-Syndrom ; Toxisch epidermale Nekrolyse ; Antikonvulsiva-Hypersensitivitäts-Syndrom ; Carbamazepin ; Key words Erythema exsudativum multiforme majus ; Stevens-Johnson syndrome ; Toxic epidermal necrolysis ; Anticonvulsant hypersensitivity syndrome ; Carbamazepin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A 28 year old patient developed a severe bullous exanthem and enanthem combined with hepatitis, fever and blood count abnormalities after taking carbamazepine and consumption of heroin and alcohol. After discontinuing carbamazepine, prednisolone was given over a five day period accompanied by intravenous fluid and electrolyte substitution and local therapy which lead to improvement. Severe bullous skin reactions nowadays are classified into erythema exsudativum multiforme majus (EEMM), Stevens-Johnson syndrome (SJS), overlap Stevens-Johnson syndrome-toxic epidermal necrolysis (SJS/TEN), TEN with maculae and TEN on large erythema, and they are most often caused by antibiotics and anticonvulsant drugs. Heroin and alcohol abuse alters host immunity which subsequently may increase susceptibility to allergic reactions. There is a high (40%) mortality rate for TEN, and patients with organ involvement are at increased risk.
    Notes: Zusammenfassung Wir berichten über einen 28jährigen Patienten, bei dem es nach Alkohol- und Heroinkonsum unter gleichzeitiger Carbamazepin-Medikation zu einem schweren bullösen Exanthem und Schleimhautenanthem verbunden mit Hepatitis, Fieber und Blutbildveränderungen kam. Nach Carbamazepin-Karenz erfolgten eine 5tägige systemische Prednisolon-Therapie unter Flüssigkeits- und Elektrolytsubstitution sowie lokale Behandlungsmaßnahmen, was zur Besserung führte. Schwere bullöse Hautreaktionen werden heute in Erythema exsudativum multiforme majus (EEMM), Stevens-Johnson-Syndrom (SJS), SJS mit Übergang in toxisch epidermale Nekrolyse (SJS/TEN) sowie TEN mit Maculae und TEN auf großflächigem Erythem eingeteilt, und neben Antibiotika gehören Antikonvulsiva zu den häufigsten Auslösern. Eine Veränderung der Abwehrlage durch Alkohol und Heroin kann offensichtlich die allergische Reaktionsbereitschaft erhöhen. Die Mortalität der TEN ist mit 40% hoch, und besonders gefährdet sind Patienten mit zusätzlicher Organbeteiligung.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001050051004
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    Paper (German National Licenses)
    Fulltext
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