After giving an overview of the general pathology of endotoxin mediated diseases the authors summarize the endotoxin induced endocrine changes and their clinical consequences, with particular regard to reproduction. Forced, premature luteolysis with formation of short-lived corpora lutea in cyclic non-pregnant individuals as well as with embryonal loss in the corpus luteum dependent phase of pregnancy might be attributed to the temporary activation of cyclooxygenase-2 and lipoxygenase enzyme systems resulting in elevated release of various prostanoids (Table) in ruminants, sows and mares. The clinical relevance of this phenomenon, however, is strongly influenced by the species- dependent duration of the prostaglandin F2α-insensitive period in the corpus luteum phase in cyclic animals and by the endocrine characteristics of pregnancy in different species. Both the experimental administration of endotoxin and the natural out-break of an endotoxin mediated disease (for example Gram-negative mastitis) are always followed by an about 24 h long elevation in peripheral level of glucocorticoids to which clinical importance is attributed in the down-regulation of certain inflammatory mediators, mainly of α-tumor necrosis factor. This increased cortisol level may interfere, however, also with the baseline and preovulatory LH secretion resulting in alterations in the follicular growth. The clinical failures attributable to endotoxin induced changes in thyroid function and in peripheral level of some other hormones (prolactin, growth hormone and insulin-like growth factor 1) are also reviewed shortly.
|Number of pages||7|
|Journal||Magyar Allatorvosok Lapja|
|Publication status||Published - Dec 1 1998|
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