Objective To assess the occurrence of chronic hypertension and renal disorder after gestations complicated by pregnancy induced hypertension or pre‐eclampsia and to define background factors and laboratory analyses at follow up examination which discriminate between women who remain normotensive and those who develop hypertension. Setting Swedish university hospital. Subjects Women with pregnancy induced hypertension (PIH) (n= 49), pre‐eclampsia (n= 45) or a normotensive pregnancy (n= 44) during 1986. Design Subjects were reviewed in 1993 with regard to chronic hypertension and renal disorder. Plasma concentrations of creatinine, urea, uric acid, calcium and albumin were measured, and urine was examined for the presence of microalbuminuria and erythrocyte excretion rate. Those with and without hypertension at follow up were compared with regard to the renal function tests and possible features in the history which might predict chronic hypertension. Results Women with a history of pregnancy induced hypertension or pre‐eclampsia had an increased risk, relative to controls, for hypertension at follow up (37% and 20%vs 2%; P < 0.001), microalbuminuria (14% and 20%vs 2%; P < 0.05) and demonstrated increased plasma levels of albumin corrected calcium (2.41 [SE 0.021 and 2.40 [0.01] vs 2.32 [0.01] mmol/l; P < 0.001). The only factors significantly associated with hypertension at follow up were the presence of microalbuminuria (P= 0.0008) and having had a delivery prior to the index pregnancy (P= 0.0017). Conclusions The risk for chronic hypertension seven years after a pregnancy complicated with pregnancy induced hypertension or pre‐eclampsia is considerably increased. The presence of hypertension at follow up is closely related to residual renal disorder.

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The value of the Endo-Pap endometrial cell sampling device in the cytological assessment of the endometrium was compared with fractional curettage. 318 symptomatic women were studied consecutively, among whom were 42 with malignant tumors of the uterus. Satisfactory material for cytological diagnosis of the endometrial state was obtained in 96%, whereas only 91% of the histopathological material was suitable for interpretation. 35 of 36 women with primary cancers of the corpus uteri had atypical endometrial cytology (sensitivity 0.97). Of 42 uterine cancers, including one metastatic ovarian carcinoma, two adenocarcinomas and three squamous carcinomas of the cervix, 40 were detected by endometrial cytology (sensitivity 0.95). All 5 cases of high grade cytological atypia in endometrial polyps or endometrial hyperplasia could be diagnosed by abnormal endometrial cytology and 4 of 5 patients with adenomatous endometrial hyperplasia were diagnosed correctly. Endometrial cytology obtained with the Endo-Pap sampler is a simple and cheap diagnostic method with which to detect endometrial cancer. It is also effective for diagnosis of preinvasive endometrial lesions with highgrade cytological atypia. Clinicians should recognize that out-patient investigation of the endometrial state by endometrial cell sampling with the Endo-Pap is reliable and can usually replace fractional curettage.

Serum levels of sex hormone binding globulin (SHBG) and testosterone (T) and bone mineral density (BMC) in the non-dominant forearm were determined in 28 postmenopausal women aged 44-62 years. Significant correlations (Spearman's rank correlation test) were found between BMC and SHBG (negative) and between BMC and the T/SHBG index on biologically active androgen (positive). Significant correlations were also found between endometrial pathology (Kruskal-Wallis test; 0 = atrophic, 1 = hyperplasia, 2 = cancer) and SHBG (negative) and the T/SHBG index (positive). It is suggested that SHBG may act as one common denominator in the pathogenesis of postmenopausal osteoporosis and endometrial disease by regulating the levels of unbound, biologically active androgens and estrogens.