scholarly journals Pharmacotherapy for female nocturia

2021 ◽  
Vol 64 (6) ◽  
pp. 449-454
Author(s):  
Soo Rim Kim

Background: In 2018, nocturia and nocturnal lower urinary tract function definitions were updated in a clinically and practically based consensus report by the International Continence Society Standardization Steering Committee. Previous research has suggested that the pathophysiology of nocturia has a multifactorial etiology, including obstructive sleep apnea, overactive bladder syndrome, diabetes mellitus, sleep disturbance, congestive heart failure, primary polydipsia, and other factors.Current Concepts: Three main mechanisms have been identified: low functional bladder capacity, nocturnal polyuria, and diurnal polyuria (24-hour polyuria). Multifactorial pathophysiology implies multiple possible targets for therapeutic intervention, and suggests that it is unlikely that one treatment modality, including drugs, will be successful in all patients. The bladder diary is the most important diagnostic tool.Discussion and Conclusion: Strong evidence supports the efficacy of desmopressin and continuous positive pressure breathing. Antimuscarinic drugs for treating nocturia display limited usefulness because of their low efficacy for nocturnal polyuria. Management of nocturia may require a multidisciplinary approach to visualization and phenotyping of patients for diagnosis and therapy.

Author(s):  
Angelo Canora ◽  
Carmine Nicoletta ◽  
Giacomo Ghinassi ◽  
Dario Bruzzese ◽  
Gaetano Rea ◽  
...  

There is evidence that hypopneas are more common than apneas in obstructive sleep apnea (OSA) related to idiopathic pulmonary fibrosis (IPF). We investigated the frequency distribution of hypopneas in 100 patients with interstitial lung diseases (ILDs) (mean age 69 yrs ± 7.8; 70% males), including 54 IPF cases, screened for OSA by home sleep testing. Fifty age- and sex-matched pure OSA patients were included as controls. In ILD-OSA patients the sleep breathing pattern was characterized by a high prevalence of hypopneas that were preceded by hyperpnea events configuring a sort of periodic pattern. This finding, we arbitrarily defined hyperpnea–hypopnea periodic breathing (HHPB), was likely reflecting a central event and was completely absent in control OSA. Also, the HHPB was highly responsive to oxygen but not to the continuous positive pressure support. Thirty-three ILD-OSA patients (42%) with a HHPB associated with a hypopnea/apnea ratio ≥3 had the best response to oxygen with a median residual AHI of 2.6 (1.8–5.6) vs. 28.3 (20.7–37.8) at baseline (p < 0.0001). ILD-OSA patients with these characteristics were similarly distributed in IPF (54.5%) and no-IPF cases (45.5%), the most of them being affected by moderate–severe OSA (p = 0.027). Future studies addressing the pathogenesis and therapy management of the HHPB should be encouraged in ILD-OSA patients.


1995 ◽  
Vol 79 (4) ◽  
pp. 1278-1285 ◽  
Author(s):  
C. Cahan ◽  
M. J. Decker ◽  
J. L. Arnold ◽  
E. Goldwasser ◽  
K. P. Strohl

The effect of nasal continuous positive pressure (CPAP) treatment on erythropoietin (EPO) was examined by measuring diurnal serum EPO levels before and twice (over the 3rd day and over 1 day on recall after > or = 1 mo of therapy) after initiation of treatment in 12 obstructive sleep apnea syndrome patients with normal hemoglobin, hematocrit, creatinine, blood urea nitrogen, and albumin levels. Over each study day, oxygen saturation was measured by an ambulatory pulse oximetry system. Patients spent 27 +/- 9% (SE) of time below oxygen saturation of 88% vs. 2.1 +/- 0.6% after initiation of nasal CPAP treatment (P < 0.01). The number of desaturation events per hour of sleep before nasal CPAP treatment was 62 +/- 6 vs. 9 +/- 2 with nasal CPAP (P < 0.01). EPO levels measured by radioimmunoassay were drawn every hour before and at 3 days (n = 9) and before and at recall (n = 0) after initiation of CPAP therapy. The mean serum EPO level was higher before treatment (61 +/- 14 mU/ml) than that at 3 days (38 +/- 10 mU/ml, P < 0.01) or at recall (32 +/- 7 mU/ml, P < 0.01). We conclude that nasal CPAP treatment of sleep-disordered breathing will reduce diurnal levels of EPO.


Drug Research ◽  
2017 ◽  
Vol 67 (05) ◽  
pp. 302-307 ◽  
Author(s):  
Asao Tanioka ◽  
Takashi Deguchi

AbstractWe evaluated the pharmacological characteristics of KRP-103, chemically named as ((2-(4-acetylpiperazin-1-yl)-6-[3,5-bis(trifluorometheyl)-phenylmethyl]-4- (2-methylphenyl)-6,7,8,9-tetrahydro-5H-pyrimido[4,5-b][1,5]oxazocin-5-one), and its effects on lower urinary tract function in guinea pigs. In radioligand binding assay, KRP-103 showed higher selectivity for human NK1 receptor (hNK1R) than for human NK2 receptor (hNK2R) and human NK3 receptor (hNK3R) (Ki for hNK1R, hNK2R and hNK3R=0.126 nM, > 10 000 nM and > 10 000 nM). In distention-induced rhythmic bladder contractions (RBCs) in urethane-anesthetized guinea pigs, intravenous administration of KRP-103 dose-dependently increased the shutdown time of RBCs and slightly decreased the amplitude of RBCs (only about 20%). In acutely spinalized guinea pig cystometory, intraduodenal administration of KRP-103 dose-dependently increased the effective bladder capacity with a minimum effective dose of 1 mg/kg. Furthermore, to clarify the site of action of KRP-103, we evaluated the inhibitory effects of KRP-103 on bladder contractions induced by electrical stimulation (ES) of the central or peripheral cut end of the pelvic nerve (PN). KRP-103 inhibited the bladder contractions induced by ES of the central cut end of PN but not those induced by ES of the peripheral cut end of PN. These results indicate that KRP-103 enhances bladder storage function by inhibiting sensory transmission from the bladder at the level of spinal cord without affecting bladder efferent function, suggesting that KRP-103 may be a suitable therapeutic drug for treatment of overactive bladder.


Sign in / Sign up

Export Citation Format

Share Document