. Is LUF a Primary granulosa cell defect??

Some case of  luteinized unruptured follicle syndrome are believed to be primary defect of Granulosa cell(lack of FSH receptors in the follicular epithelial cells)

. But where is the evidence which would account for Primary granulosa cell defect?? Can we predict it well ahead??.  1) Initial slow follicular growth, 2) absent primary progesterone rise and 3) reduction in blood flow in the wall of the follicle after the LH surge are points in favour of primary granulosa cell defect. .4) Late Bloomers –In such cases growth of the leading follicle will be usually slow during the follicular phase of the cycle. After the luteinizing hormone (LH) surge,  growth of the follicle will be more likely to be more rapid in cases which are destined to be LUF . Concurrently, 5)  the follicle later develops internal echogenicity with ultrasonic evidence of separation of the granulosa cell layer. 6 ) Later those which has turned into  LUF the follicle will be  no longer visible after 144 hours and 132 hours  after the LH rise and peak respectively. 7) There will be no primary progesterone rise associated with either the LH rise or peak, but these cases will have a secondary progesterone rise occurred 42 hours after the onset of the LH surge. 8) Moreover those who are destined to develop LUF there will have  a definite Peri-follicular blood flow velocity detected for the first time on cycle day 5 and appeared to rise after the onset of the LH surge. But unfortunately, peri-follicular blood flow velocity will appear to reduce after the LH surge to values associated with the follicular phase.

These observations are usually seen in LUF cases and may predict LUF well ahead possibly before Trigger.Whatever it may be the above features of slow growth of D F(late catch up-late bloomer) & reduction in blood flow in the wall of the follicle after the LH surge  are  consistent with an association of a primary granulosa cell defect with luteinized unruptured follicle syndrome which would account for the initial slow follicular growth, absent primary progesterone rise and reduction in blood flow in the wall of the follicle after the LH surge. A Peri-follicular blood flow velocity was detected for the first time on cycle day 5 and appeared to rise after the onset of the LH surge. Peri-follicular blood flow velocity appeared to reduce after the LH surge to values associated with the follicular phase. These observations are consistent with an association of a primary granulosa cell defect with luteinized unruptured follicle syndrome which would account for the initial slow follicular growth, absent primary progesterone rise and reduction in blood flow in the wall of the follicle after the LH surest