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Leptin is a hormone involved in the regulation of body weight and sexual maturation. We previously reported that cancer cachexia was associated with reduced or normal levels of leptin. Here we investigate whether leptin levels are related to cachetic or hormonal status. Circulating leptin and its mRNA from adipose tissue were measured in 87 patients with gynaecological and breast cancers and related to tumour, cachexia and hormonal markers. We found that leptin protein increased in patients with these tumours due to higher mRNA levels. In patients with ovarian cancer, the increased leptin levels were associated with higher circulating follicle-stimulating hormone (FSH). The higher leptin concentrations in patients with endometrial and portio tumours were related to an increase in tissue estrogen receptor (ER) and progesterone receptor (PGR) and, only in the postmenopause, to an increase in circulating estradiol. Patients with breast cancer showed enhanced blood plasma concentrations of progesterone and estradiol, and enhanced tissue levels of ER and PGR associated with increased leptin levels. The data from the present study indicate that, in gynaecological and breast cancers, leptin is related to hormonal status but not to cachexia. We suggest that leptin stimulates the production of sexual hormones, important risk factors for these tumours, and we propose leptin as a novel prognostic marker.

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Carboplatin is used in many kind of tumors with similar results to cisplatin but without the same toxicity. We decided to use it, in combination with etoposide, for metastatic breast cancer. Eighteen women with advanced breast disease entered this phase II study. Each of them received, every 28 days, carboplatin on day 1, at a dose calculated with the Calvert formula, and etoposide on days 1, 2, 3 at a dose of 100 mg/m2. For 12 women this treatment was the first-line chemotherapy, while for the other six it was the second-line therapy, after the administration and the failure, in 4 cases out of 6, of regimens based on anthracycline. In each group we obtained an objective response of 50%, with a complete response of 25% in the first and of 33% in the second. On the whole, 11 patients died (one not from the disease) (10/18, 55%). Toxicity was extremely mild, with only one patient with grade III anemia. Our data suggest that a carboplatin/etoposide combination could be active and well-tolerated in patients with metastatic breast cancer, but the few number of patients in this study makes further research necessary for confirmation.

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BACKGROUND: Activated clotting time (ACT) values during percutaneous transluminal coronary angioplasty (PTCA) after the initial 10,000 U heparin bolus are often below target values of 350 or 400 s (Hemochron) and have to be supplemented with additional heparin. This study evaluated the initial 10 min post-heparin bolus clotting time value using a body surface area (BSA)-adjusted heparin bolus versus the traditional 10,000 U heparin bolus. HYPOTHESIS: Body surface area adjustment of initial heparin dosing prior to PTCA will be more effective in reaching target ACT values compared with the 10,000 U heparin bolus method. METHODS: Twenty-seven patients receiving the BSA-adjusted heparin bolus were compared with 27 age- and gender-matched controls who had received the traditional heparin bolus. The adjusted heparin bolus formula used was [BSA(m2)/1.3m2] x 10,000 U of heparin. RESULTS: The success rate at reaching the target value of 400 s was 13 of 27 (48.1%) and 2 of 27 (7.4%) for the BSA-guided and 10,000 U heparin-guided groups, respectively (p < 0.01). The success rate at reaching the 350 s target value was 25 of 27 (92.6%) and 6 of 27 (22.2%) for the BSA-guided and 10,000 U heparin-guided groups, respectively (p < 0.01). The 95% confidence intervals for the difference in success between the BSA-guided and 10,000 U heparin-guided groups were 0.19-0.62 and 0.52-0.89 for the 400 s and 350 s ACT targets, respectively. CONCLUSION: Body surface area adjustment of initial heparin dosing is a more effective method of reaching the initial ACT target values of 350 and 400 s compared with the traditional method prior to PTCA. This conclusion applies to the Hemochron ACT device and arterial samples, and adjustments may need to be made for other devices and/or venous samples.

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When arterial blood samples for activated clotting time (ACT) are difficult to obtain from the arterial sheath during coronary intervention, venous ACT serves as a substitute. Data are lacking on whether arterial and venous ACT are identical and whether one can serve as an effective substitute for the other. Forty-eight patients undergoing percutaneous transluminal coronary angioplasty (PTCA) were prospectively evaluated to answer this question. Simultaneous arterial and venous ACT samples were drawn from femoral artery and vein vascular sheaths before and during each procedure, and ACT values were determined with a Hemochron automated electronic timer. Porcine heparin dosing was guided by arterial ACT in the first 25 patients and by venous ACT in the last 23 patients. The target ACT value used for continued heparin dosing was 400 sec. At baseline and throughout the study up to 60 min, venous ACT was slightly and significantly greater than arterial ACT. Despite this statistical difference in ACT values, there was no difference in complication rate between the two groups, and the amount of heparin used during either guiding regimen was the same. Therefore, although venous ACT values are slightly higher than arterial, the more convenient venous ACT can be safely used to guide heparin dosing during PTCA when using a target ACT value of 400 sec.

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Thirty patients with frequent (greater than or equal to 30/hr) and repetitive ventricular premature beats (VPBs) unassociated with acute infarction were randomized to intravenous lorcainide (LOR) or lidocaine (LID). Following at least 2 hours of baseline Holter monitoring, patients received LOR, 2 mg/kg then 200 mg/24hr, or LID, 1 mg/kg then 2 mg/min, with rebolus if needed. Nonresponders detected by bedside telemetry were crossed over. Clinical response was 6 of 25 (24%) including two of nine crossovers with LOR and 8 of 26 (31%) including 3 of 12 crossovers with LID (p = NS). By computer analysis of 24-hour Holter monitors and asymptotic regression of success rates at hourly intervals, it was projected that greater than or equal to 80% reduction in VPBs occurred in 28% of LOR and in 25% of LID (p = NS), and complete suppression of repetitive VPBs occurred in 102% of LOR and in 92% of LID (p = NS). The mean drug levels were 405 ng/ml (range 371 to 463) with LOR and 3.4 micrograms/ml (range 2.1 to 3.6) with LID. Side effects were similar, occurring in 8 of 25 LOR trials and in 11 of 26 LID trials (p = NS). Thus, LOR and LID effectively suppress repetitive VPBs and to a lesser extent VPB frequency. However, neither drug is superior and each may be an effective alternative when resistance to the other is encountered.

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