PubMed · 15999767
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Hiroshi Yamasaki, Hideyuki Sasaki, Machi Furuta. 2005. [Bladder dysfunction in diabetics].. https://pubmed.ncbi.nlm.nih.gov/15999767/
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A 62-year-old woman with axonal Guillain-Barré syndrome developed weakness and urinary retention simultaneously. The retention failed to recover for 10 months even after she regained the ability to walk. The patient exhibited no postural hypotension. Videourodynamics showed that the retention was caused not by the bladder paralysis but rather by internal (sympathetic) sphincter obstruction, which is extremely uncommon in peripheral neuropathies. We started the patient on an alpha-adrenergic antagonist, urapidil, at 30 mg/day, and this led to successful relaxation of the urethra and reduced the postvoid residual from 200 ml to less than 30 ml. The underlying mechanisms of urinary retention in our patient appeared to involve hyperactive lumbosacral sympathetic nerves. Urinary retention and sympathetic sphincter obstruction can thus be features of axonal Guillain-Barré syndrome.
The purpose of this study was to evaluate the effect and investigate the putative mechanism of botulinum toxin type A (BTA) applied to the treatment of benign prostatic hyperplasia (BPH). A total of 52 patients with symptomatic BPH were evaluated. Transperineal intraprostatic injection under transrectal ultrasonography was carried out. BTA dissolved in 4 to 9 mL of saline was used from 100 U to 300 U, according to prostate volume. Twenty-six patients received only BTA (BT group), and 26 received both BTA and one month of an alpha-adrenergic antagonist (BTalpha group). The therapeutic outcomes were evaluated by comparing parameters such as international prostate symptom score (IPSS), quality of life, prostate specific antigen, prostate volume, post-void residual urine, and peak urinary flow rate. At the one month follow- up, 18 patients in the BT group and 21 in the BTalpha group had subjective symptomatic relief (p = 0.337). Only IPSS5 (weak stream) was significantly different between the BT group and BTalpha groups (p = 0.034). At the three month follow-up, 39 patients had subjective symptomatic relief. The storage symptoms were improved more than the voiding symptoms. Additionally, about 50 percent of the patients whose voiding symptom improved expressed improved erectile function. BTA injection seems to be an alternative treatment for BPH. The differences after the one month evaluation between the BT and the BTalpha groups might suggest that the adrenergic influence could be relatively reinforced by the anticholinergic effect of BTA. Nitric oxide would thus be involved in a BTA action mechanism in BPH.
BACKGROUND: In experimental brain death models, autonomic storm (AS) triggers severe myocardial dysfunction, which can be attenuated by pharmacologic treatment. The aim of this study was to determine the incidence of AS in a cohort of human organ donors and to evaluate the potential interest of AS treatment on myocardial function, cardiac harvesting and transplantation. METHODS: The cohort consisted of 152 patients. Among them, 46 patients were initially considered as potential cardiac donors (main criteria: age < 60 years, no history of cardiac disease). AS diagnosis included increased systolic arterial pressure > 200 mm Hg associated with tachycardia >140 beats/min. Heart acceptance criteria were associated creatine kinase (CK), troponin Ic, and left ventricle ejection fraction (LVEF) estimated by echocardiography and visual inspection. RESULTS: AS was observed in 29 patients (63%). Hypertension was treated in 12 patients (esmolol n = 6, urapidil n = 5, nicardipine). Cardiac harvesting was performed in 28 donors (61%). LVEFs were significantly higher after AS treatment (no AS: 55.4 +/- 13.4%, untreated AS: 49.0 +/- 18.8%, treated AS: 63.9+ +/- 10.3%, P = 0.049). AS treatment was found to be independently associated with LVEF in > 50% of the cases (P = 0.034). Treatment of AS or the lack of AS were associated with an increased probability of successful cardiac transplantation (OR = 8.8; 95% CI 2.1-38.3, P = 0.002). CONCLUSIONS: Treatment of hypertension during AS may attenuate brain death-induced myocardial dysfunction and increase the number of available cardiac grafts.