Linked Life Data

6596911

Source:http://linkedlifedata.com/resource/pubmed/id/6596911

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1985-3-8
pubmed:abstractText
Menstrual blood was collected from five eumenorrheic and seven dysmenorrheic women aged between 20 and 35 years for a period of three cycles each. The levels of prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-k-PGF1 alpha)-the stable metabolite of prostacyclin (PGI2)-, oestradiol, oestrone, and progesterone were determined radioimmunologically. Both eumenorrheic and dysmenorrheic women showed identical blood losses. The levels of oestradiol excreted by the dysmenorrheic women were markedly elevated as compared to the non-dysmenorrheic subjects (2 p less than 0.05). Oestrone excretion was in the same order of magnitude in all subjects examined. The concentration of progesterone per menstruation was significantly higher in the eumenorrheic women (2 p less than 0.02) than in the dysmenorrheic patients. Menstrual excretion of PGF2 alpha was 2.5 times higher in the dysmenorrheic women compared to the normal subjects (2 p less than 0.05). The levels of PGE2 was identical in both groups. Excretion of 6-k-PGF1 alpha was significantly lower in the dysmenorrheic women than in the eumenorrheic subjects (2 p less than 0.02). The oestradiol/progesterone ratio showed a distinct predominance of oestradiol in the dysmenorrheic patients. PGF2 alpha dominance in the dysmenorrheic patients is expressed by the PGF2 alpha/6-k-PGF1 alpha and the PGF2 alpha/PGE2 ratios. A shift in the oestradiol/progesterone ratio in favour of oestradiol seems to be the underlying pathogenic principle of dysmenorrhea. The oestradiol dominance is associated with a shift in the PGF2 alpha/PGI2 and the PGF2 alpha/PGE2 proportions. Thus, the PGF2 alpha predominance and a simultaneous reduction of PGI2 in uterine tissue seem to be responsible for dysmenorrheic bleeding.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0170-9925
pubmed:author
pubmed:issnType
Print
pubmed:volume
236
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
99-108
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Contribution to the pathogenesis of dysmenorrhea.
pubmed:publicationType
Journal Article