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Biomedical subjects

C Campagnoli

Publications and source records attributed to C Campagnoli.

At least 19 recordsLinked to original sources
PubMed1998

Aspects of progestin activity on the breast. European Progestin Club.

On 9-11 May 1997, the second Meeting of the European Progestin Club was held in Turin, Italy. Aspects of progestin use on the breast were discussed, based on the currently available scientific data. The paper covers topics addressed at the meeting and summarizes the recommendations which could be agreed on by the participants.

Breast↗
PubMed1998

Insulin-like growth factor I (IGF-I) serum level modifications during transdermal estradiol treatment in postmenopausal women: a possible bimodal effect depending on basal IGF-I values.

The objective of this study was to determine the influence of transdermal estradiol administration on insulin-like growth factor I (IGF-I) serum level in a series larger than those published to date. Thirty-nine postmenopausal women with vasomotor symptoms were studied; blood samples (after overnight fast) were obtained just before and at the 6th month of treatment with transdermal estradiol 0.05 mg/day, and serum levels of IGF-I, growth hormone and sex hormone binding globulin (SHBG) were evaluated. Sixteen of the 39 women did not show variations of IGF-I values (group A), while 11 showed an increase (group B) and 12 showed a decrease (group C) by at least 20% with transdermal estradiol treatment. IGF-I basal levels were higher in group C as compared to group A (p < 0.05) and to group B (p < 0.01), intermediate in group A, and lower in group B. Group C showed a significant increase of SHBG values with transdermal estradiol treatment. Transdermal estradiol seems to induce a bimodal effect on IGF-I serum levels, depending on IGF-I basal values. This could be caused by a different responsivity to estrogen action on the liver (the major site of circulating IGF-I production) and also, possibly, by a different degree in insulin sensitivity changes caused by estrogen.

Administration, Cutaneous↗
PubMed1997

Efficacy and tolerability of Estraderm MX, a new estradiol matrix patch.

OBJECTIVES: To assess the efficacy and tolerability of a new matrix patch delivering 0.05 mg estradiol per day (Estraderm MX 50) in postmenopausal women with moderate to severe postmenopausal symptoms. METHODS: A multicenter, double-blind, randomized, between-patient, placebo controlled trial in 109 postmenopausal women was carried out. Patches were applied twice weekly for 12 weeks. Patients were assessed at 4, 8 and 12 weeks of treatment. The primary efficacy variable was change from baseline in mean number of moderate to severe hot flushes (including night sweats) per 24 h during the last 2 weeks of treatment. Other variables included Kupperman Index, local and systemic tolerability. Plasma concentrations of estradiol (E2), estrone (E1) and estrone sulfate (E1S) were determined before and after treatment. RESULTS: Estraderm MX was significantly superior to placebo (P < 0.001) in reducing mean number of moderate to severe hot flushes (including night sweats) per 24 h after 4, 8 and 12 weeks of treatment. The estimate of treatment group differences after 12 weeks was 4.2 hot flushes (95% confidence interval: 2.6-5.8). Estraderm MX also significantly reduced Kupperman Index at all time points compared to placebo (P < 0.001). Estraderm MX induced increases in mean E2, E1 and E1S plasma levels as expected (E2: baseline 2.7 pg/ml, 12 weeks 38.9 pg/ml; E1: baseline 18.8 pg/ml, 12 weeks 41.6 pg/ml; E1S: baseline 235.6 pg/ml, 12 weeks 765.1 pg/ml). Overall rates of adverse experiences were similar for Estraderm MX and placebo. The number of patients reporting skin irritation was low and similar in both groups. CONCLUSIONS: Estraderm MX 50, a new matrix patch, offers an effective and well tolerated dosage form for transdermal delivery of 0.05 mg E2 per day.

Administration, Cutaneous↗
PubMed1997

Noninvasive prenatal diagnosis. Use of density gradient centrifugation, magnetically activated cell sorting and in situ hybridization.

OBJECTIVE: To develop a noninvasive method suitable for clinical prenatal diagnosis. STUDY DESIGN: Fetal nucleated erythrocytes were separated from peripheral blood of 17 healthy pregnant women using small magnetically activated cell sorting columns (MiniMACS) following density gradient centrifugation and dual antibody labeling methods. The protocol was designed to compare the efficacy of antitransferrin receptor (CD71)/antiglycophorin A (GPA) antibodies with antithrom-bospondin receptor (CD36)/anti-GPA antibodies in identifying nucleated erythrocytes in maternal blood. Cytospin preparations of the isolated cells were subjected to in situ hybridization with specific DNA probes for the Y chromosome and chromosome 21 to confirm the fetal origin. RESULTS: After MiniMACS the enrichment factors for the CD71/GPA- and CD36/GPA-positive cells from maternal blood were similar, and the percentages of fetal cells recovered did not differ. Seven of seven male pregnancies were correctly identified. One case of trisomy 21 was detected. CONCLUSION: The in situ hybridization analysis of fetal nucleated erythrocytes isolated from maternal blood using single density gradient centrifugation, anti-CD71/anti-GPA immunostaining and MiniMACS could be an accurate, sensitive and noninvasive method for prenatal diagnosis.

Cell Separation↗
PubMed1997

Lipid profile during hormone replacement therapy: effect of different progestins?

Oral estrogens cause a decrease of low density lipoprotein cholesterol (LDL-chol.) and, especially an increase of high density lipoprotein cholesterol (HDL-chol.) levels, which both have potentially favorable effects; they also cause a triglyceride level increase, which probably has no clinical relevance except in cases with basal hypertriglyceridemia. Transdermal estradiol causes generally a minor decrease in LDL-chol. and minor increase HDL-chol. levels, with no increase or even decrease in triglyceride levels. The addition of androgenic progestins at conventionally used doses, while not interfering with LDL-chol. variations, causes a HDL-chol. decrease, which contrasts the effect of oral estrogens and completely reverses the effect of transdermal estradiol. On the contrary, the addition of a non androgenic progestin does not interfere with any of the estrogen induced lipid profile modifications.

Cholesterol, HDL↗
PubMed1997

Effect of progestins on IGF-I serum level in estrogen-treated postmenopausal women.

Insulin-like growth factor I (IGF-I) has a role in the whole-body anabolism and promotes both normal and abnormal cell growth in several tissues. Although IGF-I is also synthesized locally at numerous other sites, the liver does constitute the major site of its synthesis, and circulating IGF-I is mainly of hepatic derivation. The production of IGF-I is stimulated by growth hormone (GH), the secretion of which is influenced by circulating IGF-I level through a negative feed-back mechanism. Oral estrogen treatment causes a significant decrease of the IGF-I serum level, probably through a hepatocellular effect due to the first hepatic passage. Treatment with transdermal estradiol (tdE2) at the currently used doses does not cause, on average, substantial variations in the IGF-I serum level. The addition of an androgenic progestin--with strong hepatocellular actions, opposite to those of estrogen--completely reverses the IGF-I decrease induced by oral estrogens, and even causes a trend to IGF-I increase when tdE2 is used. Conversely, the addition of a non androgenic progestin, like dydrogesterone, does not cause interference with the estrogen effect.

Administration, Cutaneous↗
PubMed1997

Progestins and breast cancer risk.

There is still no clear account on the role that progestins play in human breast cancer, and the issue continues to be debated. The effects of progestins on breast cell proliferation have been investigated in a number of different experimental systems with conflicting results. Progesterone has been reported to both stimulate and inhibit the growth of experimental mammary tumors, depending upon the dose and the experimental models. Epidemiological studies on the effect of combined hormone replacement therapy (HRT) on breast cancer risk in menopausal women are limited because the use of a progestin in addition to estrogens was not widely adopted until 10 years ago. Taking meta-analysis into account estrogen-progestin use did conclude that there is not an excess risk in combined HRT users. Epidemiological studies have provided conflicting results, ranging from a protective effect to a deleterious effect of progestin addition on breast cancer risk. Progestins include a large family of molecules characterised by different binding capacities to androgen receptors. This implies that they should be considered as distinct yet related, therapeutic agents. The use of different progestins may account for the controversial results obtained in studies conducted in different geographic areas.

Animals↗
PubMed1995

Potential impact on breast cancer risk of circulating insulin-like growth factor I modifications induced by oral HRT in menopause.

Unlike parenteral estrogens, oral estrogen administration in menopause causes, through its hepatocellular action, a significant decrease of circulating insulin-like growth factor I (IGF-I) levels; this effect is opposed by the addition of an androgenic progestogen. In vitro studies show that IGF-I is a potent mitogen for 'estrogen responsive' breast cancer cells. Moreover, some findings in breast cancer patients and in women treated with tamoxifen suggest that reduction of circulating IGF-I could be protective to the breast. However, by also considering (1) the potential action on breast cancer cells of IGF-II, (2) the possible consequences of the growth hormone (GH) increase caused by the IGF-I reduction and (3) the fact that in vitro results are not simply transferable to the in vivo condition, other 'scenarios' can be envisaged, besides the favorable one. In support of the latter, there are epidemiologic data which suggest that oral estrogen use could have some favorable peculiarities with regards to breast cancer risk. The associated decrease in circulating IGF-I level could well be one of these peculiarities.

Breast Neoplasms↗
PubMed1994

Karyotype in myelodysplastic syndromes: relations to morphology, clinical evolution, and survival.

One hundred eighty-eight unselected consecutive patients with "de novo" myelodysplastic syndrome (MDS) were studied cytogenetically. They were subclassified as 4 refractory anemia with ringed sideroblasts (RARS), 67 refractory anemia (RA), 58 refractory anemia with excess of blasts (RAEB), 40 RAEB in transformation (RAEB-t), and 19 chronic myelomonocytic leukemia (CMML). The overall incidence of chromosome abnormalities was 69%. The RAEB and RAEB-t patients showed karyotypic changes, more often than RA and CMML (76% and 100% vs. 56% and 42%, respectively). The most frequent single anomaly was del(5)(q13-q22q33) (22 cases), followed by monosomy 7 or del 7q (11 cases), del(11) (q14q23) (8 cases), trisomy 8 (4 cases). Complex karyotypes (defined by the presence of three or more structural or numerical abnormalities) were detected in 33 patients. With regard to the FAB classification, del (5)(q13q33) was associated with RA, and complex rearrangements with RAEB and RAEB-t. Leukemic transformation occurred in 66 patients (46%), none with a normal karyotype or del(11)(q14q23) as single abnormality. In patients carrying 5q- alone, acute evolution correlated with proximal breakpoint localization, being found in no case with del(5)(q13q33) but in three out of four cases with del(5)(q22q33). Acute leukemia (AL) progression happened in all cases with complex rearrangements and monosomy 7 or del(7q). Two of the four trisomy eight patients evolved in AL. By using the Cox proportional hazard regression analysis it was demonstrated that the karyotype abnormality was a significant predictor of leukemic transformation (P < 0.001). Patients with abnormal karyotypes without complex abnormalities had a survival (median survival 12 months) shorter than that of cases with only normal metaphases (median 83 months) (P < 0.001); patients with a mixture of normal/abnormal metaphases had a median survival of 31 months. The median survival for complex karyotypes was 7 months. Among cases with single defects, del(5)(q13q33) showed the best survival (64 months), monosomy 7 and del(7q) the worst (7 months) (P < 0.001).

Chromosome Mapping↗
PubMed1994

Androgenic progestogens oppose the decrease of insulin-like growth factor I serum level induced by conjugated oestrogens in postmenopausal women. Preliminary report.

Oral oestrogen treatment in postmenopausal women causes a decrease of insulin-like growth factor I (IGF-I) serum level, probably through a hepatocellular effect. To explore the possibility that the androgenic progestogens oppose this effect, serum IGF-I and sex hormone binding globulin (SHBG) were evaluated in two groups of patients treated respectively with oral conjugated oestrogens (oCE) or transdermal oestradiol (tdE2), in a first phase with the addition of dydrogesterone (DYDR), a non-androgenic progestogen, and subsequently with the addition of norethisterone acetate (NETA). With respect to basal values, treatment with oCE+DYDR caused an increase of SHBG (P < 0.002) and a decrease of IGF-I serum levels (P < 0.05); the shift to NETA addition opposed both effects: SHBG levels decreased partially but significantly (P < 0.01 vs. oCE + DYDR) and IGF-I returned to basal values with a significant increase with respect to the oCE + DYDR phase (P < 0.02). No changes were observed in the tdE2 + DYDR treated women; in this group the shift to NETA addition caused a significant decrease of SHBG values (P < 0.001 vs. before treatment and vs. tdE2 + DYDR phase) and a slight increase of IGF-I values. These differential effects on IGF-I and SHBG serum levels might be relevant as far as breast cancer risk is concerned.

Administration, Cutaneous↗
PubMed1994

Maternal and fetal platelet activation in normal pregnancy.

OBJECTIVE: To study the platelet activation phase in normal pregnant women and their fetuses, both in vivo under basal conditions and in vitro after stimulation by adenosine diphosphate (ADP), a weak agonist, and U46619, a strong one. METHODS: Platelet function was investigated in 39 normal pregnant women and their fetuses undergoing fetal blood sampling at 18-37 weeks' gestation, using flow cytometry and the anti-GMP140 monoclonal antibody. This combined technique allows platelets to be investigated in small aliquots of whole blood, and it detects platelet secretion regardless of aggregation. In all cases, the percentage of activated platelets was determined under basal conditions and after addition of platelet agonists: ADP at concentrations of 10 and 50 mumol/L, and U46619, a stable analogue of thromboxane A2, at 1 mumol/L. RESULTS: Compared to nonpregnant controls, pregnant women had a significantly lower percentage of activated platelets after addition of U46619 (P = .02). Compared to their mothers, fetuses had significantly inferior platelet activation after addition of both platelet-activating factors at all concentrations used (ADP 10 mumol/L, P < .0001 and ADP 50 mumol/L, P < .0001; U46619, P < .0001). Maternal and fetal platelet activation did not change with duration of gestation. In the fetus, the percentage of activated platelets did not correlate with hematocrit, pH, or oxygen pressure, but it correlated significantly with platelet count after addition of U46619 (r = 0.45, P = .006). CONCLUSIONS: Decreased platelet activation in both pregnant women and fetuses suggests the action of a plasma factor that selectively inhibits prostaglandin-dependent activation. Prostacyclin, which is known to decrease platelet aggregation and release reactions caused by agonists, might have a greater inhibitory effect in the fetus than in the mother, or be present in larger amounts in the fetus.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Long-term hormone replacement treatment in menopause: new choices, old apprehensions, recent findings.

In recent years there has been an increase in the use of parenteral oestradiol as an alternative to the conventional oral preparations used in hormone replacement treatment (HRT) in menopause, such as conjugated equine oestrogens (CEE). The latter have been subject in the past to apprehensions, partly due to misunderstanding and oversimplification but also in relation to problems that have arisen during the history of HRT, for example the increase in endometrial cancer risk deriving from the use of non-progestogen-opposed treatment. However, confidence in long-term HRT comes from the epidemiological findings, which refer mainly to the use of oral CEE unopposed by progestogen: a reduced risk of osteoporotic fractures and of cardiovascular disease, and a very limited risk of breast cancer. Oral oestrogens produce marked hepatocellular effects. These effects are, on the whole, favourable from the point of view of cardiovascular risk. In addition, it cannot be excluded that some hepatocellular effects of oral oestrogen, for example increased sex hormone binding globulin levels and reduced circulating insulin-like growth factor I activity, offer protection to the breast. As progestogen supplementation is needed in non-hysterectomized women, priority should be given to preparations, such as progesterone or dydrogesterone, that feature good endometrial activity without opposing oestrogen hepatocellular effects.

Estradiol↗
PubMed1993

Differential effects of oral conjugated estrogens and transdermal estradiol on insulin-like growth factor 1, growth hormone and sex hormone binding globulin serum levels.

In postmenopausal women oral ethinylestradiol causes a reduction in circulating insulin-like growth factor 1 (IGF-1) and an increase in serum growth hormone levels. There are no data on the effect of conjugated estrogens, the preparation most often used in estrogen replacement treatment (ERT), on these parameters. We evaluated serum IGF-1 and growth hormone levels, together with the levels of sex hormone binding globulin (SHBG), an indicator of estrogen hepatocellular action, before and after 6 months of ERT in two comparable groups of postmenopausal women. Sixteen women were treated with oral conjugated estrogens, 0.625 mg/day, and 14 with transdermal estradiol, 0.05 mg/day. In the women treated with oral conjugated estrogens, an increase in SHBG (p < 0.001), a decrease in IGF-1 (p < 0.001) and an increase in growth hormone (p < 0.05) serum levels were observed. No such effects were seen with the use of transdermal estradiol, devoid of hepatocellular effects. Undoubtedly, oral conjugated estrogens, 0.625 mg/day, through a hepatocellular effect, cause marked modifications in the IGF-1/growth hormone axis, which may have clinical relevance. For instance, the decreased IGF-1 level, together with the increased level of SHBG, might provide some explanation of the favorable epidemiological data on breast cancer risk in women receiving oral conjugated estrogens.

Administration, Cutaneous↗