Recent studies have demonstrated that short-term angiotensin converting enzyme (ACE) inhibition with captopril can reduce urinary albumin excretion rate (UAER) after exercise in normotensive diabetic patients with early-stage nephropathy. The aim of this study was to investigate whether this effect of ACE inhibition was due to a systemic hypotensive action or a specific action at the intrarenal level. Thus, we compared the acute effects of captopril and the Ca2(+)-channel blocker nifedipine on exercise-induced UAER in normotensive (blood pressure less than 165/95 mmHg) diabetic patients who were normoalbuminuric or microalbuminuric at rest (stage 2 or 3 of diabetic nephropathy). Twenty-five stage 2 diabetic nephropathy patients, 39 stage 3 diabetic nephropathy patients, and 12 nondiabetic subjects performed five submaximal cycloergometric exercises (90% of theoretical heart rate) on nonconsecutive days. The first two exercises were performed in basal conditions; the next three exercises were performed 24 h after administration of captopril (25 mg twice daily) or nifedipine AR (20 mg twice daily) or placebo (1 tablet twice daily) according to a randomized double-blind crossover trial. After placebo, blood pressure and UAER did not change at rest or 1 h after exercise. After captopril, blood pressure at rest and during exercise was similar to that observed after placebo. UAER at rest was not modified, whereas 1 h after exercise, it was significantly decreased both in stage 2 and stage 3 diabetic nephropathy patients (P less than 0.001). After nifedipine, blood pressure decreased significantly at rest and during exercise in respect to placebo and captopril. UAER at rest did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
These findings indicate that hepatocellular carcinoma-associated hypoglycemia may be due exclusively to increased glucose utilization by the tumor mass.
In this open, prospective, study were enrolled 204 hospitalized elderly patients with severe (88 males, 116 females, age range 70-94). Patients were randomized to receive one of the following antibiotic treatment regimens: meropenem 500 mg i.v. t.i.d. (52); imipenem/cilastatin 500 mg i.v. t.i.d. (51), clarithromycin 500 mg + ceftriaxone 1 g i.v. b.i.d. (52), clarithromycin 500 mg + amikacin 250 mg i.v. b.i.d. (49). In 99 cases causative germs were isolated (24 meropenem, 26 imipenem, 23 clarithromycin + ceftriaxone, 26 ceftriaxone + amikacin). A satisfactory clinical, bacteriological response was achieved respectively in 86.5% 77% in meropenem; 86.3% 71% in imipenem/cilastatin; 69% 61% in ceftriaxone + clarithromycin and in 85.7% 77% in clarithromycin + amikacin. The mean total cost for each patient was $1,560; $1,620; $1,760 and $1,792 in meropenem, imipenem/cilastatin, clarithromycin + ceftriaxone and clarithromycin + amikacin respectively. This study shows that treatment with either meropenem or imipenem is as efficacious as conventional therapy in the treatment of community acquired pneumonia (CAP), and that meropenem is the most cost-effective.
Residual B-cell function was assessed in 61 type I and 17 type II insulin-treated diabetics by measuring plasma C-peptide concentration before and after i.v. injection of 1 mg glucagon to evaluate a possible difference in response to the test in the two groups. Fasting and post-stimulatory C-peptide levels were significantly higher in type II diabetics than in type I (0.45 +/- 0.25 vs 0.12 +/- 0.10 nmol/l for basal IRCP, 0.39 +/- 0.19 vs 0.06 +/- 0.11 nmol/l for delta IRCP, p less than 0.0001), but there was some overlap in individual values. Twenty-one percent of type I and 29% of type II diabetics had values in the overlap area. These percentages were reduced to 6% and 12%, respectively when only long-term (duration of diabetes more than five years) type I diabetics were considered. These data indicate that a glucagon test is useful to discriminate most type I diabetics from insulin-treated type II diabetics.
In three open, multicentre, prospective randomised studies, the efficacy and safety of meropenem were assessed and compared with ceftazidime (Study 1) and imipenem/cilastatin (Studies 2 and 3) in 864 patients; 417 with urinary tract infections (UTI) and 447 with community acquired lower respiratory tract infections (LRTI). All the antibiotics were administered by intramuscular injection. Clinical and bacteriological responses were assessed at the end of therapy and at follow-up (2-4 weeks for LRTI, 4-6 weeks for UTI). The clinical response rate in UTI at the end of therapy was 93-100% for meropenem 500 mg tds compared with 94-95% for ceftazidime 500 mg tds; for meropenem 500 mg bd it was 97%, significantly higher than that for imipenem/cilastatin 500 mg bd which was 90% (P = 0.03). At follow-up, the response rates were 90% for meropenem tds compared with 81-85% for ceftazidime 500 mg tds and 81% for meropenem bd compared with 78% for imipenem/cilastatin 500 mg bd. The clinical response rate in LRTI at end of therapy was 93% for meropenem 500 mg tds, compared with 92% for ceftazidime 1 g tds; for meropenem 500 mg bd the clinical response rate was 96%, compared with 91% for imipenem/cilastatin 500 mg bd (P = 0.054). At follow-up, the clinical response rates were 96%, 89%, 93% and 96%, respectively. The bacteriological response rates at 5-9 days post-therapy in UTI were 61-84% in patients treated with meropenem 500 mg tds, compared to 73-82% in patients treated with ceftazidime 500 mg tds; the rates for meropenem 500 mg bd and imipenem/cilastatin 500 mg bd were each 75%. At follow-up, the response rates were 40-72%, 57-70%, 51% and 49%, respectively. In LRTI, bacteriological response rates at the end of therapy were 91% for both meropenem 500 mg tds and ceftazidime 1 g tds, and 91% for meropenem 500 mg bd compared with 86% for imipenem/cilastatin 500 mg bd. At follow-up, the response rates were 87%, 77%, 84% and 79%, respectively. All treatments were well tolerated. In these studies, intramuscular meropenem proved to be an effective and well tolerated treatment for LRTI and UTI.
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