Influence of hormone replacement therapy on postmenopausal pelvic organs.

OBJECTIVE: To assess the influence of hormone replacement therapy (HRT) on the pelvic organs of postmenopausal women by vaginal ultrasonography. DESIGN: The study (case-control) included 753 consecutive, postmenopausal women who were referred for routine transvaginal ultrasound examination. A total of 290 women who were using HRT at the time of examination (study group) were compared with 463 who were not treated (control group). RESULTS: The women using HRT were younger and had been menopausal for a shorter period, compared with those who had not been treated. Mean uterine volume, endometrial thickness and ovarian area were all increased in the HRT group, compared to the control group. A negative correlation was found between menopausal age and uterine volume, and ovarian area in both treated and untreated groups. However, endometrial thickness was negatively correlated with menopausal age in the untreated group only. After controlling for various parameters, a multivariate logistic analysis demonstrated that endometrial thickness was treatment status-dependent only. Uterine volume was also treatment status-dependent, but was also negatively correlated with menopausal age. As expected, the endometrium was thicker and the uterine volume was larger in the treated group. Ovarian area was not found to be treatment-dependent for all menopausal ages. CONCLUSIONS: Postmenopausal women treated with HRT have a larger uterus and thicker endometrium than those of non-treated matched controls. There is a negative correlation between menopausal age and uterine and ovarian size. Endometrial thickness was found to be negatively correlated with menopausal age in only the untreated group, and is almost entirely HRT-dependent. In contrast to the uterus and the endometrium, the ovaries are not influenced by HRT.

Mutation analysis of the MEN1 gene in Israeli patients with MEN1 and familial isolated hyperprolactinemia.

Multiple endocrine neoplasia type 1 (MEN-1) is characterized by hyperfunction and tumor formation of the parathyroids, anterior pituitary and endocrine pancreas. We carried out exon-specific, PCR-based DNA sequencing of the coding exons of the MEN1 gene in 8 Israeli MEN1 patients: 4 familial and 4 sporadic. We similarly analyzed Israeli families with a unique phenotype of isolated hyperprolactinemia (HPRL). Four mutations were detected in 4 MEN1 patients: C to T alteration at nucleotide 2608 resulting in R108X, and three intronic insertions/deletions (a 13 basepair (bp) deletion and a 1 bp insertion both in intron 1, and a 2 bp insertion in intron 3) leading to exonic frame shifts as they encompass the splice junctions. An additional patient exhibited a compound mutation: a G to T change at position 7614 resulting in E463X, and insertion/deletion of 9 bp at position 7622-7630 resulting in EAE466-468X. Haplotype analysis showed no segregation of phenotype with 11q13 markers in 4 familial HPRL, and no men 1 germline mutations were detected in three representative individuals, from 3 families. Our results confirm that men 1 gene germline mutations occur in the majority of patients with clinically diagnosed MEN1, and that familial HPRL is a genetically distinct disorder.

In vitro modulation of activation antigens on human lymphocytes by beta-estradiol.

PROBLEM: The possible in vitro immunomodulating effect of beta-estradiol on phytohemagglutinin-stimulated human lymphocyte cultures was studied. METHOD OF STUDY: Lymphocyte cultures from 12 healthy men and women aged 25-35 years were set up for 12 hr in the presence and in the absence of beta-estradiol, and the expression of the activation markers CD25, CD69, and CD71 was examined by flow cytometric analysis with specific fluorescent conjugated antibodies. RESULTS: Although the number of cases is small, in 10 of 12 cases in the presence of beta-estradiol in two different concentrations, a significantly decreased expression of CD69 could be observed. A slight decrease could also be observed for the Interleukin-2 receptor expression; however, the difference, in the presence or absence of beta-estradiol, was not significant. CONCLUSIONS: The results suggest that in vitro addition of beta-estradiol can inhibit, to a certain degree, specific activation markers on phytohemagglutinin-stimulated lymphocytes from young men and women. The present study could not define the role of sex differences because of the small number of samples. A comparison between men and women at various ages in a greater number of cases, as well as studies on activation markers after treatments with estrogens, would be useful.

Long-term prognosis of patients with paroxysmal atrial fibrillation complicating acute myocardial infarction. SPRINT Study Group.

The aim of the study was to assess the relationship between paroxysmal atrial fibrillation during acute myocardial infarction and the long-term prognosis of patients after acute myocardial infarction. The incidence of paroxysmal atrial fibrillation among 5803 consecutive hospitalized patients was 9.9% (557/5803). Incidence rose with increasing age (less than or equal to 59 years, 4.2%), (60-69 years, 10.5%), (greater than or equal to 70 years, 16.0%) and was slightly (but not significantly) higher in women (11.0%) than in men (9.6%). The presence of congestive heart failure and mean age represented two major discriminants between patients with paroxysmal atrial fibrillation (70% and 68.6 years) in comparison with their counterparts (35% and 62.3% years). Hospital mortality was significantly higher (25.5%) in patients with paroxysmal atrial fibrillation than in those without (16.2%). However, the effect of paroxysmal atrial fibrillation disappeared when other factors influencing the short term prognosis (i.e. heart failure) were taken into account by a multivariate logistic regression analysis. The covariate adjusted relative odds of in-hospital mortality then fell to 0.82. The 1- and 5-year mortality rates were 18.6% and 43.3% in patients with paroxysmal atrial fibrillation as compared to 8.2% and 25.4% (P less than 0.001), respectively, in patients free of paroxysmal atrial fibrillation. Using a proportional hazards analysis of mortality through the first quarter of 1988 (average follow-up time, 5.5 years) the net risk of dying among patients with paroxysmal atrial fibrillation complicating the acute myocardial infarction is estimated at 1.28 (90% confidence interval, 1.12-1.46) relative to counterparts free of the complication.(ABSTRACT TRUNCATED AT 250 WORDS)