Fulminante venöse und arterielle Thrombosen unter Heparintherapie

Prull, A.; Nechwatal, Robert; Mäurer, W

doi:10.1055/s-2008-1065030

Cited by 4 publications

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Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

Sinkovics

2011

Advances in Experimental Medicine and Biology

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This article reviews the history of widespread exchanges of genetic segments initiated over 3 billion years ago, to be part of their life style, by sphero-protoplastic cells, the ancestors of archaea, prokaryota, and eukaryota. These primordial cells shared a hostile anaerobic and overheated environment and competed for survival. "Coexist with, or subdue and conquer, expropriate its most useful possessions, or symbiose with it, your competitor" remain cellular life's basic rules. This author emphasizes the role of viruses, both in mediating cell fusions, such as the formation of the first eukaryotic cell(s) from a united crenarchaeon and prokaryota, and the transfer of host cell genes integrated into viral (phages) genomes. After rising above the Darwinian threshold, rigid rules of speciation and vertical inheritance in the three domains of life were established, but horizontal gene transfers with or without cell fusions were never abolished. The author proves with extensive, yet highly selective documentation, that not only unicellular microorganisms, but the most complex multicellular entities of the highest ranks resort to, and practice, cell fusions, and donate and accept horizontally (laterally) transferred genes. Cell fusions and horizontally exchanged genetic materials remain the fundamental attributes and inherent characteristics of the living matter, whether occurring accidentally or sought after intentionally. These events occur to cells stagnating for some 3 milliard years at a lower yet amazingly sophisticated level of evolution, and to cells achieving the highest degree of differentiation, and thus functioning in dependence on the support of a most advanced multicellular host, like those of the human brain. No living cell is completely exempt from gene drains or gene insertions.

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Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

Sinkovics

2011

Advances in Experimental Medicine and Biology

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Heparininduzierte Thrombocytopenie Typ II

Eder¹,

Hamann²

1999

Chirurg

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Heparin-induced thrombocytopenia type II (HIT type II) is an immunoglobulin-mediated, drug-induced side effect for heparin-treated patients with thromboembolic complications. With an incidence of 1-3 %, mortality of 20 % it and permanent disability for another 20 % is a clinically relevant disorder. With heparin treatment or prophylaxis frequent platelet count monitoring is necessary. With HIT type II the thrombocytopenia is often a harbinger of thromboembolic complications in the venous or arterial system. If HIT type II is suspected, further heparin exposure is to be stopped immediately and another anticoagulant therapy should be started. The two anticoagulant options in Germany are discussed. At the same time the diagnosis should be confirmed by laboratory testing, including testing for cross-reactivity with danaparoid. Further therapy depends on the symptoms. In the case of clinical relevance of this disorder we should think about prophylaxis: strict indications for perioperative prophylaxis only use of low-molecular-weight heparin (LMWH) for routine prophylaxis, use of LMWH for thrombosis treatment and early change to cumarine.

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Pathomorphological aspects of heparin-induced thrombocytopenia II (HIT-II syndrome)

Hermanns¹,

Janssens²,

Handt

et al. 1998

Virchows Archiv

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The therapeutic use of heparin results in thrombocytopenia in 5-30% of patients. In 0.1-1% of patients treated with heparin, the platelet count decreases to between 100 x 10(9)/l and 50 x 10(9)/l and leads to severe synchronous central arterial and venous thrombosis with a mortality of 18-36%. This is known as "white-clot syndrome" or heparin-induced thrombocytopenia II (HIT-II syndrome). Whilst the clinical aspects and the central type of thrombosis in HIT-II syndrome are well documented, the histomorphology and differential diagnosis of thrombosis are not. We report three cases of HIT-II syndrome with thrombosis of the central arteries and veins. The HIT-II thrombi could be differentiated from thrombi of other origins, particularly from mural thrombi. Heparin-induced thrombi were seen on microscopical examination to be like onion skin in structure, and immunohistochemistry showed that they had a markedly reduced content of fibrin and clearly enhanced amounts of IgG and IgM. The layered structure thus implied appositional growth. The thrombi in HIT-II syndrome do not seem to be induced by activation of the coagulation cascade, but by platelet aggregation mediated by anti-platelet antibodies.

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Fulminante venöse und arterielle Thrombosen unter Heparintherapie

Cited by 4 publications

References 0 publications

Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

Heparininduzierte Thrombocytopenie Typ II

Pathomorphological aspects of heparin-induced thrombocytopenia II (HIT-II syndrome)

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