Analysis of multiple casualty incidents - a prospective cohort study.

BACKGROUND: Our aim was to report the rate and causes for multiple casualty incidents (MCI) to analyse the prehospital part of responding to MCIs, report mortality and find areas for improvement. METHODS: A prospective cohort study conducted in an urban emergency medical service (EMS) between 1.3.1998 and 28.2.2004. RESULTS: Fifty-nine MCIs involving 263 patients (167 walking, 96 non-walking) occurred. The incidence of MCIs was 1.8/100,000 inhabitants year(-1). Traffic accidents were the most common cause followed by residential fires, intoxications and stabbings or shootings. Early MCI alarm by the dispatching centre was performed in 18 MCIs. Deviations from standard emergency medical care occurred in 12% of patients. Lack of immobilization of the neck or back in trauma patients and lack of administration of 100% oxygen in suspected carbon monoxide intoxication were the most common deviations. Deviations were related to the lack of presence of on-scene medical command (P = 0.0013) and inadequate resources (P = 0.0342). One hundred and ninety-two patients were transported to emergency departments. Mortality during the prehospital phase was 4.9% (13/263) and during the next 28 days 2.3% (6/263). Adequate resources for safe and effective management of a MCI were related to an early MCI alarm by the dispatching centre (P = 0,022) and to the presence of on-scene medical command (P < 0,001). CONCLUSIONS: Traffic accidents, residential fires and intoxications were the leading causes for MCIs. Emergency medical service could respond to most MCIs efficiently and safely. Majority of deviations from standard medical care seemed potentially preventable. Several areas for improvement were identified. From prehospital links, the dispatching centre and on-scene medical command had a vital role in the successful management of MCIs.

Change in bone mass distribution induced by hormone replacement therapy and high-impact physical exercise in post-menopausal women.

The purpose of this intervention trial was to determine whether changes in bone mass distribution could be observed in postmenopausal women following hormone replacement therapy (HRT) and/or high-impact physical exercise. Eighty healthy women, aged 50-57 years, at <5 years after the onset of menopause and with no previous use of HRT, were randomly assigned to one of four groups: HRT; exercise (Ex); HRT + Ex (ExHRT); and control (Co). HRT administration was conducted in a double-blind manner for 1 year using estradiol plus noretisterone acetate (Kliogest). The exercise groups participated in a 1 year progressive training program consisting of jumping and bounding activities. Subjects participated in two supervised sessions per week and were asked to perform a series of exercises at home 4 days/week. Bone measurements using a quantitative computed tomography scanner (Somatom DR, Siemens) were obtained from the proximal femur, midfemur, proximal tibia, and tibial shaft. Data were analyzed with a software program (BONALYSE 1.3) calculating density (g/cm(3)), cross-sectional area (CSA; mm(2)), and moments of inertia (I(max), I(min), I(polar)). In addition, the bone mass spectrum was determined as a function of the angular distribution around the bone mass center (polar distribution) and the distance from the bone mass center through the diaphyseal wall (radial distribution). After the 1 year period, there was an overall interaction of group x time in bone mineral density (BMD) at the proximal femur (p = 0.05) and tibial shaft (p = 0.035). Women in the ExHRT and HRT groups had increased proximal femur and tibial shaft BMD when compared with the change observed in the Co group (p = 0.024-0.011). The change was more pronounced in the cortical tibia, wherein the ExHRT group also differed from the Ex group (p = 0.038). No significant changes were found in bone CSA at any of the measured sites. The radial distribution indicated an increase of BMD in the endocortical part of the measured sites in the HRT and ExHRT groups and in the proximal tibia in the Ex group. The polar distribution showed that bone mass was redistributed in the anteroposterior direction. The changes in I(max), I(min), and I(polar) in the HRT and ExHRT groups differed from those in the Co group at the proximal femur, midfemur, and proximal tibia (p = 0.047-0.001). The Ex group also differed from the Co group in I(max) and I(polar) at the proximal tibia (p = 0.018 and 0.039, respectively). These results support the idea that HRT acts primarily at the bone-marrow interface. The exercise intervention chosen for this study contributed to the maintenance of bone mass. Our results suggest that both HRT and exercise have local effects on bone mass. The change in bone mass distribution induced by HRT and exercise may play an important role in the alteration of bone strength.

Effects of hormone replacement therapy and high-impact physical exercise on skeletal muscle in post-menopausal women: a randomized placebo-controlled study.

An age-related decline in muscle performance is a known risk factor for falling, fracture and disability. In women, a clear deterioration is observed from early menopause. The effect of hormone replacement therapy (HRT) in preserving muscle performance is, however, unclear. This trial examined the effects of a 12-month HRT and high-impact physical exercise regimen on skeletal muscle in women in early menopause. A total of 80 women aged 50-57 years were assigned randomly to one of four groups: exercise (Ex), HRT, exercise+HRT (ExHRT) and control (Co). The exercise groups participated in a high-impact training programme. The administration of HRT (oestradiol/noretisterone acetate) or placebo was carried out double-blind. Knee extension torque and vertical jumping height were evaluated. Lean tissue cross-sectional area (LCSA) and the relative proportion of fat within the muscle compartment were measured for the quadriceps and lower leg muscles. The ExHRT group showed significant increases in knee extension torque (8.3%) and vertical jumping height (17.2%) when compared with the Co group (-7.2%). Vertical jumping height also increased after HRT alone (6.8%). The LCSA of the quadriceps was increased significantly in the HRT (6.3%) and ExHRT (7.1%) groups when compared with the Ex (2.2%) and Co (0.7%) groups. Lower leg LCSA was also increased in the ExHRT group (9.1%) when compared with the Ex (3.0%) and Co (4.1%) groups. In addition, the increase in the relative proportion of fat in the quadriceps in the Co group (16.6%) was significant compared with those in the HRT (4.9%) and ExHRT (-0.6%) groups. Thus, in post-menopausal women, muscle performance, muscle mass and muscle composition are improved by HRT. The beneficial effects of HRT combined with high-impact physical training may exceed those of HRT alone.

Plasma endothelin in postmenopausal women with type 2 diabetes mellitus and metabolic syndrome: a comparison of oral combined and transdermal oestrogen-only replacement therapy.

AIM: Type 2 diabetes and metabolic syndrome are major cardiovascular risk factors in postmenopausal women, but the role of vasoconstrictive endothelin-1 (ET-1) in these conditions is not known. We studied the levels of ET-1 and the effect of postmenopausal hormonal therapy on ET-1 levels in postmenopausal women. METHODS: We compared plasma levels of ET-1 in 22 postmenopausal type 2 diabetic women and 14 postmenopausal women with metabolic syndrome with plasma levels in 10 healthy postmenopausal control women. The basal values for ET-1 were measured for all groups. These women were then randomised to receive in a double-dummy, crossover trial: either oral continuous oestradiol (2.0 mg) + norethisterone acetate (1.0 mg) per day or continuous transdermal oestrogen-only (50 mg/day) for 3 months. Between the active therapy there were 3-month wash-out periods. ET-1-values were measured again at the end of each treatment period. RESULTS: The type 2 diabetic women had significantly (p < 0.003) elevated ET-1 levels (4.8+/-1.0 pg/ml) whereas those with metabolic syndrome (4.4+/-1.7 pg/ml]) had non-significantly (NS) elevated ET-1 levels compared to controls (3.6+/-0.3 pg/ml). Both oral and transdermal hormone replacement therapy (HRT) failed to affect plasma ET-1 except in 14 hypertensive women from the diabetes and metabolic syndrome groups who were on angiotensin convertase enzyme (ACE) inhibitors. These women's ET-1 levels before oral HRT (4.6+/-1.1 pg/ml) fell to 4.1+/-0.9 pg/ml (p < 0.05). CONCLUSIONS: Type 2 diabetes in postmenopausal women is associated with elevated ET-1 levels. Oestrogen replacement therapy does not affect the levels of ET-1 in postmenopausal women with type 2 diabetes or metabolic syndrome.

p21/WAF1 expression as related to p53, cell proliferation and prognosis in epithelial ovarian cancer.

The role and prognostic value of the tumour suppressor p21/WAF1 expression in epithelial ovarian cancer has not yet been defined. Therefore, the expression of p21/WAF1 was assessed immunohistochemically (IHC) in 316 epithelial ovarian malignancies in relation to p53, cell proliferation and patient survival. p21/WAF1 expression was inversely correlated with p53 and cell proliferation. Low p21/WAF1 expression was significantly associated with high grade of the tumour (P = 0.0005), advanced FIGO stage (P = 0.001) and primary residual tumour (P = 0.0001). Low p21/WAF1 expression was a marker of poor overall survival (P = 0.012). Similarly, p53-positivity and high cell proliferative activity were significant predictors of poor survival in univariate analyses. Moreover, the patients with p21-/p53+ tumours had a poorer overall (P < 0.00005) and recurrence-free (P = 0.0005) survival in univariate analyses, and the p21/p53 expression independently predicted tumour recurrence in Cox's multivariate analysis. Our results suggest that p21/WAF1 expression is mostly p53-dependent in epithelial ovarian cancer. High p21/WAF1 expression seems to function as a negative cell cycle regulator and as a marker of favourable disease outcome in epithelial ovarian cancer. In addition, the patients with their tumour expressing no or low p21/WAF1 protein but positive for p53 had a notably higher risk of recurrent disease, implicating that these patients might be more prone to treatment failures.

Clinical significance of alpha-catenin, collagen IV, and Ki-67 expression in epithelial ovarian cancer.

PURPOSE: To analyze alpha-catenin and collagen IV expression in epithelial ovarian cancer with special reference to their prognostic significance and correlations with clinical and pathologic characteristics, as well as cell proliferation marker Ki-67. PATIENTS AND METHODS: Alpha-catenin, collagen IV, and Ki-67 expression was immunohistochemically analyzed in paraffin-embedded specimens of 316 patients with epithelial ovarian cancer. RESULTS: Alpha-catenin and collagen IV expression was not interrelated or related to International Federation of Gynecology and Obstetrics (FIGO) stage or proliferation marker Ki-67. Alpha-catenin expression was reduced (< 100%) in 50% of primary tumors. Reduced alpha-catenin and collagen IV expression was directly related to high histologic grade (P < .001). In both univariate and multivariate analyses, Ki-67 proliferation significantly predicted overall survival. In the subset of 86 patients with stage I tumor, a reduced (< 100%) alpha-catenin expression approached statistical significance as a negative prognostic factor (P = .035) and retained its statistical significance in the multivariate analysis (P = .025). The low (< 30%) expression of alpha-catenin (n = 10) was a sign of inferior survival as compared with normal expression in both the univariate (P = .0107) and multivariate analyses (P = .0105). CONCLUSION: Alpha-catenin expression seems to be a useful marker of those FIGO stage I tumors likely to run a less favorable course. The high cell proliferative activity was associated with poor survival. In the future, alpha-catenin and Ki-67 expression should be studied in a large prospective cohort that includes early-stage cancers to select the more aggressive tumors for intense early chemotherapy.

Open randomised study of use of levonorgestrel releasing intrauterine system as alternative to hysterectomy.

OBJECTIVES: To assess whether the levonorgestrel intrauterine system could provide a conservative alternative to hysterectomy in the treatment of excessive uterine bleeding. DESIGN: Open randomised multicentre study with two parallel groups: a levonorgestrel intrauterine system group and a control group. SETTING: Gynaecology departments of three hospitals in Finland. SUBJECTS: Fifty six women aged 33-49 years scheduled to undergo hysterectomy for treatment of excessive uterine bleeding. INTERVENTIONS: Women were randomised either to continue with their current medical treatment or to have a levonorgestrel intrauterine system inserted. MAIN OUTCOME MEASURE: Proportion of women cancelling their decision to undergo hysterectomy. RESULTS: At 6 months, 64.3% (95% confidence interval 44.1 to 81.4%) of the women in the levonorgestrel intrauterine system group and 14.3% (4.0 to 32.7%) in the control group had cancelled their decision to undergo hysterectomy (P < 0.001). CONCLUSIONS: The use of the levonorgestrel intrauterine system is a good conservative alternative to hysterectomy in the treatment of menorrhagia and should be considered before hysterectomy or other invasive treatments.

Responses of HDL subclasses, Lp(A-I) and Lp(A-I:A-II) levels and lipolytic enzyme activities to continuous oral estrogen-progestin and transdermal estrogen with cyclic progestin regimens in postmenopausal women.

Seventy postmenopausal women took part in the study. Subjects received either continuous oral 17 beta-estradiol 2 mg/day combined with norethisterone acetate 1 mg/day (E2/NETA, Kliogest) or transdermal treatment consisting of 28 day cycles with patches delivering 17 beta-estradiol 50 micrograms/day (Estraderm) combined with cyclic medroxyprogesterone acetate 10 mg/day (E2/MPA, Provera), on days 17-28. At baseline the serum lipid and lipoprotein concentrations, composition and concentrations of high density lipoprotein (HDL) subclasses, lipoprotein (Lp)(AI) and Lp(A-I:A-II) levels were comparable in the two groups. In the E2/NETA group, after 12 months hormone replacement therapy (HRT), the HDL2 cholesterol concentration decreased by 17% (P < 0.01) and the HDL3 cholesterol remained unchanged. The concentrations of HDL2b, HDL2a and HDL3a were reduced by 30, 26 and 15%, respectively, P < 0.001, and the cholesterol:triglyceride ratio decreased significantly in all HDL subclasses. Apolipoprotein (apo) A-I concentration decreased by 5% (P < 0.05), but apo A-II, Lp(A-I) and Lp(A-I:A-II) concentrations remained unchanged. In the E2/MPA group the HDL2 and HDL3 cholesterol levels were both reduced by 6% (P < 0.05) and the HDL3a, HDL3b and HDL3c concentrations decreased by 14, 12 and 17% during the E2/MPA phase compared with baseline (P < 0.01). No major changes in the composition of HDL subclasses occurred in the E2 MPA group during treatment. The apo A-I and Lp(A-I) levels were not changed, but apo A-II and Lp(A-I:A-II) concentrations decreased by 8 and 5%, P < 0.001 and P < 0.05, respectively. At 12 months the postheparin plasma hepatic lipase (HL) activity decreased only in the E2/NETA group (by 12%, P < 0.05). The cholesteryl ester transfer protein (CETP) activity was not affected by either HRT regimen. The results of our study show that the 2 HRT regimens have multiple effects on HDL particles and HRT induced changes in HDL are not associated with changes in activities of lipolytic enzymes or CETP.

Effective obstetric paracervical block with reduced dose of bupivacaine. A prospective randomized double-blind study comparing 25 mg (0.25%) and 12.5 mg (0.125%) of bupivacaine.

BACKGROUND: To study whether paracervical block (PCB) with 12.5 mg (0.125%) of bupivacaine is as effective as with 25 mg (0.25%) and if there are differences in fetal heart rate (FHR) patterns between the doses. METHODS: A prospective, randomized double-blind study. Fifty-two patients received PCB with 25 mg and 45 patients with 12.5 mg of bupivacaine. Pain intensity was assessed by the patients on a horizontal visual analog scale (VAS). Fetal heart rates of the fetuses were analyzed visually concerning basal rate, variability, accelerations, bradycardia, silent pattern and decelerations. RESULTS: The pain relief was statistically significant in both groups up to 120 min after PCB. The VAS-values were similar in both groups both before and after PCB. Fetal heart rate changes appeared in both groups more frequently after than prior to PCB. In patients receiving 25 mg of bupivacaine there appeared to be more FHR changes than in those receiving 12.5 mg. CONCLUSIONS: Paracervical block with 12.5 mg of bupivacaine is an effective method to relieve pain during labor. Fetal heart rate changes seemed to appear less frequently with this reduced dose. It seems that by lowering the dose of bupivacaine it is possible to reduce fetal side-effects without losing analgesic effect.

Different effects of oral and transdermal hormonal replacement on prostacyclin and thromboxane A2.

OBJECTIVE: To elucidate the mechanism of cardiovascular protection of hormone replacement therapy (HRT) by comparing the effect of oral and transdermal HRTs on the production of antiaggregatory, vasodilatory prostacyclin, and its endogenous antagonist, thromboxane A2. METHODS: Oral estradiol (2.0 mg/d) plus norethisterone acetate (1.0 mg/d) (n = 13) or transdermal estradiol (50 micrograms/d) plus medroxyprogesterone acetate (10 mg/d) as 12-day courses at 4-week intervals (n = 13) were given to postmenopausal women. Urinary excretion of the metabolites of prostacyclin, ie, 6-ketoprostaglandinF1 alpha and 2,3-dinor-6-ketoprostaglandinF1 alpha, as well as those of thromboxane A2, ie, thromboxane B2 and 2,3-dinor-thromboxane B2, were measured by radioimmunoassays, after purification by extraction and high performance liquid chromatography, before and during the sixth and the 12th treatment cycles. RESULTS: Oral HRT stimulated excretion of thromboxane B2 from 3.4 +/- 0.7 ng/mmol creatinine to 4.5 +/- 1.5 (mean +/- standard deviation, P < .05) and that of 2,3-dinor-thromboxane B2 from 16.6 +/- 8.0 ng/mmol creatinine to 26.2 +/- 10.7 (P < .01), and thus led to the dominance of thromboxane A2. No changes in prostanoids occurred during transdermal HRT. CONCLUSIONS: The effects of various HRTs on prostanoids may significantly differ.

Different effects of continuous oestrogen-progestin and transdermal oestrogen with cyclic progestin regimens on low-density lipoprotein subclasses.

Seventy-five postmenopausal women were randomly allocated to receive either continuous oral 17 beta-oestradiol 2 mg day-1 and norethisterone acetate 1 mg day-1 (E2/NETA) or transdermal treatment consisting of 28-day cycles with patches delivering 17 beta-oestradiol 50 micrograms day-1 combined with oral cyclic medroxyprogesterone acetate 10 mg day-1, on days 17-28 (E2/MPA). At baseline, the plasma lipid and lipoprotein concentrations, composition and concentrations of low-density lipoprotein (LDL) subclasses (LDL1, LDL2 and LDL3) isolated by density-gradient ultracentrifugation were similar in the two groups. The post-heparin plasma hepatic lipase activity (HL) correlated inversely with the percentage of total LDL found in LDL1 (buoyant LDL) and directly with the percentage of LDL found in LDL3 (dense LDL). After 12 months of hormone replacement therapy (HRT), the total and LDL-cholesterol concentration of the E2/ NETA group decreased by 14% and 17% respectively (P < 0.001), while in the E2/MPA group these parameters remained unchanged. The lowering of LDL-cholesterol in the E2/NETA group was a consequence of a significant reduction of the large, buoyant LDL particles (LDL1) from 103 mg dL-1 to 60 mg dl-1 (P < 0.001) and of a decrease of cholesterol content of LDL particles in the major LDL subclass, LDL2. In the E2/MPA group, the concentration of LDL1 decreased, but less than in the oral group. In both groups, a significant increase in the concentration of the LDL3 subclass was observed, indicating an overall shift to denser LDL particles. After 12 months, the post-heparin plasma HL activity decreased only in the E2/NETA group (by 12%). The inverse correlation between post-heparin plasma HL activity and LDL1 persisted in both groups, but the direct correlation between HL and LDL3 vanished in the E2/NETA group and subsided in the E2/MPA group. Our results indicate that HRT has multiple effects on LDL subclasses and suggest that these changes cannot be explained by changes in HL activity.

Hormone replacement therapy lowers plasma Lp(a) concentrations. Comparison of cyclic transdermal and continuous estrogen-progestin regimens.

To study the responses of serum lipoproteins, apoproteins (apo's), and lipoprotein(a) (Lp[a]) to two frequently used hormone replacement therapies (HRTs), 120 postmenopausal women were randomly allocated to receive either transdermal therapy consisting of 28-day cycles with patches that delivered 17 beta-estradiol (50 micrograms/d) combined with cyclic oral medroxyprogesterone acetate (10 mg/d for 12 days per cycle) or continuous oral 17 beta-estradiol (2 mg/d) together with norethisterone acetate (1 mg/d) for 12 months. Blood samples were taken before and at 6 and 12 months of HRT. Concentrations of serum total, low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol decreased by 14% (P < .001), 17% (P < .001), and 9% (P < .001) in the oral HRT group. Respective changes were 5.7% (P < .001), 4.8% (P < .05), and 4.7% (NS) in the transdermal group. Serum triglycerides remained unchanged in the oral group but decreased by 15.7% (P < .001) in the transdermal group. We observed only trivial changes in serum apo B levels. The changes in apo A-I levels paralleled those of HDL cholesterol in the oral HRT group. The concentration of serum Lp(a) decreased by 31% (P < .001) and 16% (P < .001) in the two groups. The combination of progestin and transdermal estrogen was not associated with any further change of Lp(a). The decrement in Lp(a) during therapy was positively associated with baseline Lp(a) levels in both groups (r = .96, P < .001 and r = .88, P < .001). Thus, both HRT regimens were highly effective in lowering elevated Lp(a) levels in postmenopausal women. The divergent responses of LDL and HDL cholesterol in the two HRT groups may influence the potential cardioprotective effects of the two HRT regimens. Prospective trials are needed to define the long-term effects with respect to coronary heart disease risk.

Effects of postmenopausal estrogen/progestin replacement therapy on LDL particles; comparison of transdermal and oral treatment regimens.

The aim of the study was to compare the effects of continuous oral estrogen/progestin therapy to the effects of transdermal estrogen therapy combined with cyclic oral progestin on the properties of LDL particles. Eighty postmenopausal women were randomly allocated to receive either oral (continuous 17-beta-estradiol 2 mg and norethisterone acetate 1 mg per day, E2/NETA) or transdermal therapy (patches delivering continuous 17-beta-estradiol, E2, 0.05 mg/day with sequential oral medroxyprogesterone acetate, MPA, 10 mg/day for 12 days/cycle). The groups had similar mean values and ranges of age, BMI and postmenopausal status. The blood samples were taken at baseline, and twice at 1 year before and after MPA administration. LDL particle size distribution was determined by gradient gel electrophoresis and LDL was isolated by sequential ultracentrifugation for compositional analyses. Concentrations of total LDL mass, LDL cholesterol and LDL protein decreased in the oral treatment group (p < 0.01, p < 0.001 and p < 0.01, respectively), whereas they remained unchanged during the transdermal therapy. Particle size of the major LDL peak remained unchanged during both transdermal and oral therapies. HDL cholesterol concentration decreased significantly in both treatment groups (p < 0.001 for both). Serum triglyceride and HDL cholesterol concentrations were the strongest determinants of LDL particle size ( r = -0.50 and r = 0.54, respectively, p < 0.001 for both). The cholesteryl esters and free cholesterol content of the LDL particles decreased in the oral treatment group (p < 0.05). Phospholipid content of LDL increased in both groups receiving either oral or transdermal therapy (p < 0.01 for both). In conclusion, oral administration of 17-beta-estradiol and norethisterone acetate caused a decrease in LDL mass by decreasing the number and cholesterol content of LDL particles. The concomitant decrease of HDL cholesterol by progestins may partly negate this beneficial effect of LDL lowering.

Postmenopausal hormonal replacement decreases plasma levels of endothelin-1.

Hormone replacement therapy (HRT) protects against cardiovascular disorders, but the mechanisms of this action are poorly understood. We assessed the plasma levels of vasoconstrictive endothelin-1 (ET-1) in 26 healthy postmenopausal women before and during HRT. The women were randomized to receive either continuous transdermal (estradiol 50 ug/24 hrs) complemented with periodic 12 days' courses with medroxyprogesterone (10.0 mg/day)(n = 13) or continuous oral estradiol (2.0 mg/day) and continuous norethisterone acetate (1.0 mg/day)(n = 13). ET-1 was measured with specific radioimmunoassay after concentrating the sample with solid phase extraction. Pretreatment plasma ET-1 (1.28 +/- 0.36 pmol/ml, mean +/- SD) in the whole study group decreased (p < 0.01) to 1.05 +/- 0.26 pmol/ml at 6 months and to 1.10 +/- 0.32 pmol/ml at 12 months of treatment. A subgroup analysis between the two HRT regimens revealed no significant differences in the response of plasma ET-1 to HRT. These first data on HRT-induced reduction in plasma ET-1 may provide a new explanation for the cardiovascular protection by HRT.

Can progestin be limited to every third month only in postmenopausal women taking estrogen?

We evaluated whether a progestin, added for 14 days every 3 months to estrogen replacement therapy, is capable of preventing the development of endometrial hyperplasia in postmenopausal women during a treatment period of 2 years. Postmenopausal women (263) in 10 hospitals and medical centers in Finland participated in this non-randomized prospective multicenter trial. The women received estradiol valerate 2 mg daily for 84 days and 20 mg of medroxyprogesterone acetate daily for days 71-84 followed by seven drug-free tablets. This regimen was repeated four times per year. The first year of treatment was completed by 227 (86%) women and the second year by 143 out of 146 women. The incidence of unscheduled and heavy bleedings was higher in women who were postmenopausal for less than 3 years. Endometrial biopsies demonstrated progestational response in 64% at 12 and 24 months, respectively. The 3 month regimen prevented development of endometrial hyperplasia but was not able to restore a hyperplastic endometrium to normal.

The effect of a heat and moisture exchange filter on sidestream spirometry in critically ill patients.

Sidestream spirometry has enabled continuous on-line monitoring of the pulmonary mechanics in intubated patients. We studied the effect of the heat and moisture exchange filter (HMEF) on the displayed spirometry values of a commercial multiparameter pulmonary monitor in 35 stable ICU patients needing mechanical ventilatory support. There were statistically significant differences in tidal volumes, airway pressures, compliances and end-tidal CO2-values between the two sites of measurements on both sides on the HMEF. The effect of the HMEF was linear in almost every patient. However, the change of the displayed values was clinically of minor importance. In conclusion, we suggest that the HMEF can be safely used between the patient and the monitoring site in routine ventilatory monitoring of ICU patients.

Circulating lipid and lipoprotein concentrations during danazol and high-dose medroxyprogesterone acetate therapy of endometriosis.

In a study on endometriosis, ten patients were treated with danazol (200 mg three times a day) and ten patients with high-dose medroxyprogesterone acetate (MPA) (100 mg a day) for 6 months. The circulating high-density lipoprotein-cholesterol concentration decreased significantly in the danazol (53%) and in the MPA groups (26%); the change in the danazol group was significantly higher than that in the MPA group. Danazol also significantly increased the low-density lipoprotein-cholesterol levels (37%), whereas MPA had no significant effect. Danazol (29%) and MPA (12%) decreased the apolipoprotein A-1 levels significantly. The decrease caused by danazol was significantly greater. Danazol also significantly decreased the apolipoprotein A-2 levels (12%) and significantly increased the apolipoprotein B levels (17%), whereas MPA had no significant effects on them. Three months after the end of medication, all values were at the pretreatment levels. The circulating cholesterol, triglyceride, and very low-density lipoprotein concentrations remained unchanged during both treatments. Danazol and high-dose MPA induced a similar significant regression of peritoneal endometriotic implants in relation to placebo. Our present results, showing that danazol, to a greater extent than high-dose MPA, is associated with changes in lipoprotein metabolism that expose the individual to an increased risk of cardiovascular diseases, suggest that high-dose MPA is preferable to danazol in the long-term treatment of endometriosis.