Disease relevance of Luteal Phase

• Discordant luteal phase biopsies (greater than or equal to 3 d "out of phase") from infertility patients exhibited delayed epithelial beta 3 immunostaining [1].
• Mean plasma oestrogen and progesterone levels were significantly higher in migraine patients than controls for most of the menstrual cycle, with the most striking differences found in the late luteal phase for progesterone [2].
• The corpus luteum function of 109 patients with benign breast disease was appreciated by way of plasma progesterone and estradiol determinations during the luteal phase [3].
• The recurrent deficiency of progesterone (P) secretion by the corpus luteum has been associated with infertility and habitual abortion and given the clinical diagnosis of luteal phase deficiency (LPD) [4].
• Toward removing uterine fibroids without surgery: subcutaneous infusion of a luteinizing hormone-releasing hormone agonist commencing in the luteal phase [5].

Psychiatry related information on Luteal Phase

• RESULTS: In the luteal phase, amplitude of core body temperature, total melatonin secretions, and amplitudes of TSH and cortisol rhythms were significantly decreased, whereas sleepiness and occurrence of slow-wave sleep during the daytime were significantly increased [6].
• The corn mouse also shows a short luteal phase, and we wanted to know whether copulation and/or lactation would release prolactin and maintain progesterone secretion in this species [7].
• It may give rise to a short period of estradiol withdrawal symptoms and it may also lead to luteal phase deficiency [8].
• For all subjects, paragraph recall scores were negatively correlated with free testosterone levels, whereas paired-associate learning was positively correlated with estradiol levels in the luteal phase [9].
• The total number of ovulations exhibited by these females during the breeding season ranged from two to six and was positively related to body weight, mean luteal phase progesterone (P) levels of normal cycles and social dominance rank [10].

High impact information on Luteal Phase

• The women receiving only mifepristone had plasma progesterone levels like those of the follicular phase (less than 3 nmol per liter) within four days, whereas all the other women had plasma progesterone levels characteristic of the luteal phase (greater than 8 nmol per liter) for at least seven days after treatment [11].
• Subcutaneous injection of 50 micrograms of a long-acting analog of luteinizing hormone-releasing factor on each of two successive days during mid-luteal phase in normally cycling women induced a short luteal phase and premature menstruation [12].
• RESULTS: Maximum (mean [SD]) millisecond increase in QTc after ibutilide infusion was greater for women during menses (63 [13]) and the ovulatory phase (59 [17]) compared with women during the luteal phase (53 [14]) and compared with men (46 [16]; P =.002 vs menses and P =.007 vs ovulation) [13].
• Luteal phase was defined as day 15-42 from LMP [14].
• During the menstrual cycle, expression of flt was constant but that of KDR was increased in the luteal phase, at which time the cells migrated in response to VEGF [15].

Chemical compound and disease context of Luteal Phase

• Intermittent luteal phase sertraline treatment of dysphoric premenstrual syndrome [16].
• These data indicate that total estradiol measured during the luteal phase has a poor intraindividual reproducibility over time, and these findings may have important implications in studies of hormones in the etiology of chronic disease [17].
• We have investigated the ability of citalopram, a serotonin reuptake inhibitor, to alter the functional sensitivity to a neuroactive steroid during the late luteal phase in twelve women with premenstrual syndrome [18].
• The findings of this exploratory study in subjects with radiolucent and mixed gallstones suggest that men and postmenopausal women have lower LH, and premenopausal women in the luteal phase of the cycle have higher E2, than controls [19].
• Double-blind randomized crossover trial of luteal phase estrogens (Premarin) in the premenstrual syndrome (PMS) [20].

Biological context of Luteal Phase

• Two of the 16 patients were excluded from the hormone statistical analyses because the serum progesterone levels were not consistent with sampling in the luteal phase of the menstrual cycle [21].
• Previous studies of the role of estrogen in primate luteolysis, designed to investigate the effects of estrogen antagonism or selective inhibition of luteal phase estrogen production on luteal function, have ignored the impact of such treatments on secretory endometrial development [22].
• In the postpartum women, 32% of first cycles were anovulatory, and among ovulatory cycles, 73% had abnormally low luteal phase PdG excretion or short luteal phases [23].
• To study control of apoptosis in human endometrium, we examined late luteal-phase endometrial biopsies obtained in the late luteal phase for evidence of apoptosis and compared the effects of exogenous human chorionic gonadotropin (hCG) and progesterone on this process [24].
• After energy intake was adjusted for, the ratio of polyunsaturated to saturated fat (P:S) in the diet was significantly inversely associated with plasma estradiol and estrone during the luteal phase of the menstrual cycle [25].

Anatomical context of Luteal Phase

• Congenital and acquired anatomical defects of the uterine fundus and cervix, parental chromosomal rearrangements, gene mutations, antibodies to cardiolipin, and luteal phase defects each make a small contribution [26].
• Northern blot analysis of total RNA with 32P-labeled probes revealed that the level of KGF mRNA in the endometrium was 70-100-fold greater in the luteal phase or after P treatment than in untreated, E2-treated, or follicular phase animals [27].
• In corpora lutea, the Fas antigen staining became apparent in the granulosa lutein cells during the early luteal phase and intensified during the mid luteal phase, while the theca lutein cells became positive for the Fas antigen staining during the mid luteal phase [28].
• This system was used to observe the endocrine responses of the granulosa lutein cells to three different protocols of CG administration designed to mimic the normal luteal phase, early pregnancy, and early pregnancy followed by pregnancy loss [29].
• This hypothesis could explain the preferential retention of progesterone receptors in decidual cells observed immunohistochemically during the late luteal phase of the menstrual cycle, suggestive of a shift in progestogenic actions from the epithelium to the stroma [30].

Associations of Luteal Phase with chemical compounds

• Similar but weaker associations were observed for urinary estrogens and pregnanediol in the luteal phase [31].
• In the luteal phase, urinary estrone levels rose 15.2% (P = .05), estradiol levels increased 21.6% (P = .02), and estriol levels rose 29.1% (P = .03) [32].
• Prolactin interferes with the function of the corpus luteum, as was demonstrated by repeatedly finding a short luteal phase in the ovulatory cycles of two hyperprolactinaemic women after prolactin supression by bromocriptine had been discontinued [33].
• In the luteal phase, the oestriol ratio of the youngest parous women was again distinctively raised and generally the oestriol ratios of parous women were higher than those of nulliparae [34].
• Flow-mediated vasodilation and estradiol levels were lowest from the end of the luteal phase to the beginning of the menstrual phase and were highest in the follicular phase [35].

Gene context of Luteal Phase

• The constitutive presence of IL-1R tI in EEC, which was not affected by IL-1 beta, and the up-regulation of IL-1R tI mRNA by its ligand IL-1 beta in ESC isolated during the luteal phase suggest a role for the IL-1 system in human implantation [36].
• Messenger RNA (mRNA) expression of VEGF, flt-1, and KDR remained constant in the CL during the luteal phase and was lower in the regression phase [37].
• In conclusion, during maternal recognition of pregnancy, hCG prevents the normal increase in MMP-2 in the late luteal phase [38].
• There was no change in the expression of MMP-1, TIMP-1, and TIMP-2 throughout the luteal phase or after luteal rescue [38].
• Alpha-melanocyte-stimulating hormone antagonizes the inhibitory effect of corticotropin-releasing hormone on luteinizing hormone secretion during the luteal phase in normal women [39].

Analytical, diagnostic and therapeutic context of Luteal Phase

• Gastrointestinal transit time was significantly (p less than 0.01) prolonged in the luteal phase when progesterone levels were increased compared with the follicular phase [40].
• RT-PCR analysis detected mRNAs for Eph B1, B2, and B4 and ephrin B1 and B2, but not Eph B3 and B6 or ephrin B3, in human corpora lutea of the early luteal phase [41].
• Immunohistochemistry revealed that StAR staining was most prominent in thecal-lutein cells throughout the luteal phase [42].
• This cell culture system model mimics the profile of ovarian steroids and relaxin seen in serum during the nonconceptive luteal phase, although the relative magnitude of the hormones was not the same as seen in vivo [29].
• Quantitative analysis of the 4.0 kb band of mRNA throughout the luteal phase by densitometry revealed that the levels of LH receptor mRNA were low during the early luteal phase (days 3-5 of the luteal phase) [43].

References