Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
1985-3-5
pubmed:abstractText
Cyclosporine (CsA) is the first of a new order of pharmacological immune suppressants and represents a significant advance in the clinical control of graft rejection. In laboratory animals, its capacity to prolong allograft survival has been well documented, including reports of indefinite donor-specific immunological tolerance after shortterm CsA treatment. There is also evidence that CsA can inhibit the onset or progress of a variety of experimental autoimmune diseases. Underlying these properties of the drug is its capacity to selectively interfere with T helper cell activation and lymphokine production, although some direct effects on B cells have also been reported. In addition, sparing of suppressor cells may in part explain the mode of action of CsA which, at the molecular level, is not understood. CsA-induced nephrotoxicity in the rat has been extensively studied and is characterized by reversible proximal tubular cell damage. This problem may be aggravated by concomitant administration of other potentially nephrotoxic drugs, such as gentamicin, or by therapeutic agents which interfere with the metabolism of CsA. CsA is metabolized in the liver and excreted in the bile. Although the pathway of hepatic metabolism of CsA has not been precisely elucidated, animal studies suggest that agents capable of inducing metabolism of the drug CsA could be used to alleviate its nephrotoxic properties.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0065-4299
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
306-27
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:6395677-Animals, pubmed-meshheading:6395677-Antibody Formation, pubmed-meshheading:6395677-Autoimmune Diseases, pubmed-meshheading:6395677-Carcinogens, pubmed-meshheading:6395677-Chemistry, Physical, pubmed-meshheading:6395677-Cyclosporins, pubmed-meshheading:6395677-Digestive System, pubmed-meshheading:6395677-Graft Rejection, pubmed-meshheading:6395677-Graft vs Host Reaction, pubmed-meshheading:6395677-Hematopoietic System, pubmed-meshheading:6395677-Humans, pubmed-meshheading:6395677-Hypersensitivity, Delayed, pubmed-meshheading:6395677-Immunosuppressive Agents, pubmed-meshheading:6395677-Kidney, pubmed-meshheading:6395677-Killer Cells, Natural, pubmed-meshheading:6395677-Liver, pubmed-meshheading:6395677-Lymphatic System, pubmed-meshheading:6395677-Lymphocyte Activation, pubmed-meshheading:6395677-Lymphokines, pubmed-meshheading:6395677-Mutagens, pubmed-meshheading:6395677-Physicochemical Phenomena, pubmed-meshheading:6395677-Skin, pubmed-meshheading:6395677-T-Lymphocytes
pubmed:year
1984
pubmed:articleTitle
Cyclosporine: immunology, toxicity and pharmacology in experimental animals.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't