Molecular pathways underlying tissue injuries in the bladder with ketamine cystitis

Xie, Xiang; Liang, Jiayu; Huang, Run; Luo, Chuang; Yang, Jiali; Xing, Hongming; Zhou, Le; Qiao, Han; Ergu, Erti; Chen, Huan

doi:10.1096/fj.202100437

Cited by 12 publications

(7 citation statements)

References 252 publications

(698 reference statements)

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“…In addition to its roles in physiological bladder functions, ATP likely contributes to bladder dysfunctions that are characterized with urinary urgency and increased voiding frequency, with or without urge incontinence. For example, ATP is increased in the urine in patients with overactive bladder (OAB) syndrome [ 11 , 12 ], interstitial cystitis and bladder pain syndrome [ 13 , 14 , 15 ], and bladder infection and inflammation [ 16 , 17 , 18 ]. Conversely, decreased intravesical ATP has been found in patients with refractory detrusor overactivity and bacteriuria [ 19 ] and in patients with underactive bladder syndrome [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Urinary ATP Levels Are Controlled by Nucleotidases Released from the Urothelium in a Regulated Manner

et al. 2022

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Adenosine 5′-triphosphate (ATP) is released in the bladder lumen during filling. Urothelial ATP is presumed to regulate bladder excitability. Urinary ATP is suggested as a urinary biomarker of bladder dysfunctions since ATP is increased in the urine of patients with overactive bladder, interstitial cystitis or bladder pain syndrome. Altered urinary ATP might also be associated with voiding dysfunctions linked to disease states associated with metabolic syndrome. Extracellular ATP levels are determined by ATP release and ATP hydrolysis by membrane-bound and soluble nucleotidases (s-NTDs). It is currently unknown whether s-NTDs regulate urinary ATP. Using etheno-ATP substrate and HPLC-FLD detection techniques, we found that s-NTDs are released in the lumen of ex vivo mouse detrusor-free bladders. Capillary immunoelectrophoresis by ProteinSimple Wes determined that intraluminal solutions (ILS) collected at the end of filling contain ENTPD3 > ENPP1 > ENPP3 ≥ ENTPD2 = NT5E = ALPL/TNAP. Activation of adenylyl cyclase with forskolin increased luminal s-NTDs release whereas the AC inhibitor SQ22536 had no effect. In contrast, forskolin reduced and SQ22536 increased s-NTDs release in the lamina propria. Adenosine enhanced s-NTDs release and accelerated ATP hydrolysis in ILS and lamina propria. Therefore, there is a regulated release of s-NTDs in the bladder lumen during filling. Aberrant release or functions of urothelial s-NTDs might cause elevated urinary ATP in conditions with abnormal bladder excitability.

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Section: Introductionmentioning

confidence: 99%

Urinary ATP Levels Are Controlled by Nucleotidases Released from the Urothelium in a Regulated Manner

et al. 2022

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“…Common transient or treatable side effects of ketamine treatment include elevated pulse and/or blood pressure, headache, nausea, anxiety, changes in vision, changes in muscle tension, and/or unwanted feelings of dissociation ( 61 ). Ketamine use over time has been linked to cystitis and bladder dysfunction ( 62 , 63 ). Serious adverse events associated with ketamine treatment in a legal setting include respiratory distress and seizure ( 64 ).…”

Section: Discussionmentioning

confidence: 99%

Ketamine for Bipolar Depression: Biochemical, Psychotherapeutic, and Psychedelic Approaches

Bennett¹,

Yavorsky²,

Bravo³

2022

Front. Psychiatry

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Bipolar disorder (type 1) is a serious and chronic psychiatric illness that can be difficult to treat. Many bipolar patients have refractory depressive episodes. Racemic ketamine, a glutamate modulator with prominent dissociate and psychedelic properties, has been demonstrated to have rapid acting antidepressant and anti-obsessional effects which may be useful for treating the symptoms of bipolar depression. Most of the existing research literature on unipolar and bipolar depression has looked at racemic ketamine in the sub-psychedelic dose range given by infusion as a stand-alone treatment (without concurrent psychotherapy). This article expands on the existing research by articulating three different paradigms for ketamine treatment: biochemical, psychotherapeutic, and psychedelic. The authors use composite clinical vignettes to illustrate different ways of working with ketamine to treat bipolar depression, and discuss a variety of clinical considerations for using ketamine with this population, including route, dose, frequency, chemical mitigators, and adverse events. Note that the conceptual paradigms could be applied to any ketamine treatment, with broad applicability beyond bipolar treatment.

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“…Chronic ketamine use or abuse has been reported to induce ulcerative cystitis with a broad spectrum of clinical symptoms ranging from polyuria, decreased bladder capacity, urgency, dysuria, nocturia, urinary incontinence and suprapubic pain to gross haematuria. Common histopathological features include the denudation of the urothelium, thickened bladder wall, lamina propria fibrosis and inflammation [33,34]. The first case of ketamine-induced cystitis was described as an abuser in 2007, and approximately 30% of ketamine abusers have been reported to suffer from urinary problems.…”

Section: Ketaminementioning

confidence: 99%

Drug-Related Cystitis: An Overview

Engin

2023

Cystitis - Updates and Challenges

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Cystitis is an inflammatory condition of the urinary bladder with infectious or noninfectious aetiologies. Chemical-induced cystitis represents a relatively highly prevalent kind of noninfectious cystitis resulting from therapeutic agents or environmental chemicals. Drug-related cystitis is a type of urotoxicity of drugs, which is a commonly underreported condition leading to impaired quality of patients’ life, discontinuation of medication and non-compliance. Drug-related cystitis can occur in several forms ranging from mild urinary symptoms to gross haematuria, which can be challenging for physicians to treat. Chemotherapeutic drugs, ketamine, tiaprofenic acid and several drugs have been reported to be associated with cystitis until now. Cyclophosphamide (CP) is an alkylating agent that leads to haemorrhagic cystitis with widespread awareness due to its high prevalence in patients under treatment intravenously. However, several currently available drugs have been also reported to induce cystitis, which may be usually ignored. Drug-related cystitis can cause emergency admissions and prolonged hospitalisation, leading to increased medical costs. Some cases of drug-related cystitis are clinically managed with established therapeutic interventions and/or prophylaxis, such as CP-induced haemorrhagic cystitis. On the other hand, standard treatment is currently unavailable for most cases. This chapter will provide current knowledge regarding the drug-related cystitis that should be taken into consideration as a potential adverse effect of drugs by physicians.

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Molecular pathways underlying tissue injuries in the bladder with ketamine cystitis

Abstract: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cited by 12 publications

References 252 publications

Urinary ATP Levels Are Controlled by Nucleotidases Released from the Urothelium in a Regulated Manner

Urinary ATP Levels Are Controlled by Nucleotidases Released from the Urothelium in a Regulated Manner

Ketamine for Bipolar Depression: Biochemical, Psychotherapeutic, and Psychedelic Approaches

Drug-Related Cystitis: An Overview

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