Morphogenesis and Histostereological Analysis of Hepatopathy Induced by Cyclophosphamide

Nepomnyashchikh, L. M.; Молодых, О. П.; Лушникова, Е. Л.; Sorokina, Yu. A.

doi:10.1007/s10517-010-0887-2

Cited by 5 publications

(2 citation statements)

References 13 publications

(14 reference statements)

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“…Non-selective activity of CP and urotoxic, nephrotoxic, and cardiotoxic side-effects of this drug and its metabolites as well as reproductive disturbances caused by CP treatment seriously limit its use of clinical practice [2,10]. The hepatotoxic effects of antitumor products can be studied during experimental modeling of these processes [1,2,8].…”

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Ultrastructurural Picture of Cyclophosphamide-Induced Damage to the Liver

et al. 2011

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We studied the ultrastructural reorganization of hepatocytes and other populations of liver cells after cyclophosphamide treatment. Single administration of cyclophosphamide was followed by significant ultrastructural changes in two major populations of liver cells (hepatocytes and sinusoidal endothelial cells). This treatment was also accompanied by reactive changes in Kupffer cells, lymphocytes, and plasma cells migrating into the spaces of Disse. Cyclophosphamide-induced spatial reorganization of hepatocytes was associated with a progressive decrease in the structural density of mitochondria, significant reduction of the smooth endoplasmic reticulum, and increase in autophagocytosis (e.g., sequestration of glycogen). Intracellular reorganization of endothelial cells was related to the following two factors: damage (necrobiosis) of some cells; and increase in metabolic processes, phagocytosis, and regenerative reactions in other cells.

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Ultrastructurural Picture of Cyclophosphamide-Induced Damage to the Liver

et al. 2011

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“…150 This drug is able to modify the microvascular architecture causing endothelial damage, 151 as shown in an experimental model on liver specimens, resulting in blood stasis and thrombosis. 152 In human studies, cardiotoxicity has been reported in patients treated with cyclophosphamide, and the association with methotrexate and fluorouracil chemotherapy may cause protein C and protein S deficiency along with enhanced PAI-1 levels. 153 However, the majority of studies that found a prothrombotic activity of cyclophosphamide are based on subjects with oncohematological diseases, often in combination with other immunosuppressive drugs and with other prothombotic risk factors.…”

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confidence: 99%

Thrombosis in Autoimmune Diseases: A Role for Immunosuppressive Treatments?

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et al. 2016

Semin Thromb Hemost

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Autoimmune diseases are not infrequently associated with arterial or venous thrombotic events. Chronic inflammation and immune system impairment are considered the main pathogenetic mechanisms. Some of the drugs used in the treatment of such diseases have been associated with an increased risk of thrombosis. On the contrary, their anti-inflammatory and immune modulator activity could correct some mechanisms leading to thrombosis. In this review, recent evidence available on this topic is examined. There is a lack of adequate studies, but available evidence suggests that glucocorticoids and high-dose immunoglobulins are associated with an increased incidence of venous thromboembolism. Although available data do not allow drawing definite conclusions and more data are needed from future studies and registries, physicians should be aware of these associations.

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