Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All pregnancy-associated tissues are capable of producing prostaglandins including PGI2 and TXA2. In normal pregnancy there is a dominance of PGI2 over TXA2 which may contribute to the maternal circulatory adaptation to pregnancy. Furthermore, both fetoplacental PGI2 and TXA2 production are important regulators of the fetal blood supply. It has been clearly established that in pre-eclampsia PGI2 production decreases in the fetoplacental tissues and quite probably also in the maternal tissues. The effect of this change may be further exaggerated by the simultaneous stimulation in pre-eclampsia of TXA2 production. The reason for PGI2 deficiency is not known. Other vasoactive agents, such as endothelin, may act in concert with prostaglandins. Relative PGI2 deficiency is likely to exist also in IUGR and lupus anticoagulant syndrome of pregnancy. In the latter, lupus anticoagulant may directly inhibit the synthesis of PGI2. One study suggests PGI2 deficiency also in early pregnancies of women with a history of repeated abortions. Prostaglandin production increases during full-term labour, and similar but smaller changes also occur in preterm labour. A silent bacterial infection may trigger the onset of preterm labour through cytokine-stimulated increase of prostaglandin production. No data were found on prostaglandin production in post-term pregnancies. That oligo-polyhydramnios is possibly prostaglandin mediated is suggested by the control of polyhydramnios by indomethacin treatment. Smoking decreases the production of PGI2 and possibly increases that of TXA2, which may lead to decreased blood flow and IUGR. Which constituent of cigarette smoke exerts this effect is not known. Ethanol consumption causes aberrations in prostaglandin metabolism which cannot be directly connected with fetal alcohol effects.
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PMID:The role of prostaglandins in obstetrical disorders. 147 99

The physiologic role of the prostaglandins is complex and not yet defined precisely. Nevertheless, these ubiquitous compounds do appear important to regulation of cell function and host defenses. The therapeutic potential of the prostaglandins seems to be immense, and their use in a wide variety of clinical conditions is just beginning. Whether they will also prove helpful clinically as modulators of the immune response is not clear. It is likely that an appropriate balance of prostaglandin endoperoxides, thromboxanes, prostacyclins, and probably the stable prostaglandins themselves is important to physiologic regulation of many organ systems and of immunologic reactions. Thus, development of drugs that selectively inhibit one or another of the prostaglandins and their allied compounds may prove fruitful in treatment of many diseases, including those associated with disordered immunity and tissue injury. Prostaglandin therapy in such diseases must proceed with caution. In recent studies addition of amantadine to prostaglandin E (PGE) treatment of NZB/W mice not only increased survival of these animals, but prevented development of circulating antibodies to nuclear constituents including native DNA. The results are encouraging, but must be balanced against the observation that deprivation of prostaglandin precursors also prevented nephritis and markedly increased surival of lupus mice. However, prostaglandins might be useful in a disorder whose course is more easily monitored than that of systemic lupus erythematosus: cutaneous vasculitis. The studies in which even oral administration of a PGE1 derivative suppressed immune complex-induced vasculitis (reversed passive Arthus reaction in rat skin) suggest that a trial of PGE1 treatment of cutaneous vasculitis would not be unreasonable.
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PMID:Prostaglandins. Their potential in clinical medicine. 743 93