Add-on treatment with 0.3 mg/day moxonidine in hypertensive patients with renal failure is well tolerated and not inferior to 20 mg/day nitrendipine with respect to the incidence of specific adverse events. The idea of a sympatholytic drug to be renoprotective is appealing but needs further evaluation.
Moxonidine is a centrally active imidazoline receptor agonist that effectively lowers blood pressure and has been shown to have beneficial effects on lipid and carbohydrate metabolism. We assessed the efficacy of moxonidine in a postmarketing surveillance study (CAMUS) conducted in 772 practices in Germany, documenting 4005 patients with hypertension, who were overweight and/or suffered from metabolic syndrome. Patients were treated with moxonidine (Cynt s ) for the first time following the baseline visit for 8 weeks. Mean blood pressure decreased from 168/97 to 141/83 mmHg for all patients and from 168/96 to 141/83 mmHg for patients with metabolic syndrome. Blood pressure reduction was particularly pronounced in patients with severe hypertension at baseline. The response rate (DBPp90 mmHg or reduction X10 mmHg) of antihypertensive treatment with moxonidine was 94.0% for all patients and 93.8% for patients with metabolic syndrome. The recommended targets for antihypertensive treatment of the German Diabetes Society/German Hypertension Society were reached by 30.5% of nondiabetics (goal: o140/90 mmHg) and by 3.6% of diabetics (goal: o130/80 mmHg) observed. After 8 weeks of treatment, patients achieved a mean weight loss of 1.4 kg, which was particularly pronounced in obese patients. The rate of patients receiving antihypertensive combination therapy was 81.1% for those with metabolic syndrome, and 63.3% for all other patients. Patients with metabolic syndrome were preferentially treated with ACE inhibitors and diuretics. We conclude that moxonidine effectively reduces blood pressure in patients with metabolic syndrome while simultaneously reducing body weight in obese patients.
Urinary incontinence is the inability to willingly control bladder voiding. Stress urinary incontinence (SUI) is the most frequently occurring type of incontinence in women. No widely accepted or approved drug therapy is yet available for the treatment of stress urinary incontinence. Numerous studies have implicated the neurotransmitters, serotonin and norepinephrine in the central neural control of the lower urinary tract function. The pudendal somatic motor nucleus of the spinal cord is densely innervated by 5HT and NE terminals. Pharmacological studies confirm central modulation of the lower urinary tract activity by 5HT and NE receptor agonists and antagonists. Duloxetine is a combined serotonin/norepinephrine reuptake inhibitor currently under clinical investigation for the treatment of women with stress urinary incontinence. Duloxetine exerts balanced in vivo reuptake inhibition of 5HT and NE and exhibits no appreciable binding affinity for receptors of neurotransmitters. The action of duloxetine in the treatment of stress urinary incontinence is associated with reuptake inhibition of serotonin and norepinephrine at the presynaptic neuron in Onuf's nucleus of the sacral spinal cord. In cats, whose bladder had initially been irritated with acetic acid, a dose-dependent improvement of the bladder capacity (5-fold) and periurethral EMG activity (8-fold) of the striated sphincter muscles was found. In a double blind, randomized, placebo-controlled, clinical trial in women with stress urinary incontinence, there was a significant reduction in urinary incontinence episodes under duloxetine treatment. In summary, the pharmacological effect of duloxetine to increase the activity of the striated urethral sphincter together with clinical results indicate that duloxetine has an interesting therapeutic potential in patients with stress urinary incontinence.
In patients with lower extremity arterial occlusion who were undergoing urokinase thrombolysis, adjunctive abciximab treatment resulted in faster thrombus dissolution and improved amputation-free survival, despite an increase in major bleeding.
A total of 214 cats with signs of feline lower urinary tract disease (FLUTD) were assessed in this study. There were 81.30% males (82.20% of them neutered) and 18.70% females (80.00% of them spayed) with an age range from 9 months to 17 years (mean 5.1 ± 3.7). Most of the cats (111; 51.90%) were diagnosed with feline idiopathic cystitis; in 57 (26.60%) cats, uroliths were detected. A urinary tract infection (UTI) as well as urethral plugs were diagnosed in 23 cats (10.75%). In 100 cats, a non-obstructive form of feline lower urinary tract disease (FLUTD) was present; in 114 cats (exclusively males) a urethral obstruction was diagnosed. Most of the cats (141; 65.90%) were indoor-housed. The cats with the UTI were significantly older when compared to the other cases of FLUTD. The most common clinical signs reported by the owners were dysuria (39.70%), oliguria/anuria (31.30%), and vomiting (24.80%). In the cats with the urethral obstruction, oliguria/anuria and non-specific systemic signs were dominant whereas in the non-obstructive form, signs of a lower urinary tract disease were more frequent. The urine specific gravity ranged from 1.008 to 1.080, while in the cats diagnosed with UTI, it was significantly lower than the other cats. Haematuria was the most common finding within the urinalysis which was diagnosed in 181 cats (84.60%): macroscopic haematuria was present in 94 patients (43.90%), microscopic haematuria was present in 87 cats (40.70%). Pyuria was found in 36 cats (16.80%). In the UTI cats, the most common bacterial isolate was E. coli. Results of our study are in agreement with previous reports of FLUTD in various countries, with idiopathic cystitis as the most common cause.
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