Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
J Pain ; 25(1): 132-141, 2024 Jan.
Article in English | MEDLINE | ID: mdl-37549775

ABSTRACT

Guidelines recommend consideration of modification, tapering, or discontinuation of long-term, full-agonist opioid therapy when harms outweigh benefits; one alternative to tapering or discontinuing full-agonist opioids for the management of chronic pain is switching to the partial agonist buprenorphine. As the use of buprenorphine for pain expands, understanding the patient experience during and after the transition to buprenorphine is critical. We conducted 45- to 60-minute semistructured qualitative interviews with 19 patients to understand the experiences of patients with chronic pain actively maintained on buprenorphine after previously receiving full-agonist, long-term opioid therapy. Patients were recruited from 2 medical centers via provider referral. Through thematic analysis, 5 overall themes were identified, including satisfaction with buprenorphine, the importance of preconceptions about buprenorphine, experiences with transitions, patient-provider communication, and potential contributions to racial disparities in pain care. While we heard a range of experiences, most patients were satisfied with buprenorphine, reporting either equivalent pain control to their previous regimens or reporting less analgesia but improved functioning due to a reduction in side effects (eg, mental clarity). Patients also emphasized the importance of a nonjudgmental, patient-centered approach, including education about the risks and benefits of buprenorphine. The few Black patients interviewed all reported limited access to pain care, which is consistent with the well-documented existence of racial disparities in access to pain treatment. As buprenorphine is used more frequently for pain management, provider education focused on pain treatment disparities, patient-centered approaches informed by motivational interviewing, and increasing acceptance of buprenorphine as an option for pain are needed. PERSPECTIVE: Qualitative analyses of patient experiences transitioning from full-agonist opioids to buprenorphine for chronic pain revealed general satisfaction. Patients reflected on functioning, tradeoffs between analgesia and side effects, patient-centered care, and access to treatment, highlighting how future research should focus on outcomes valued by patients.


Subject(s)
Buprenorphine , Chronic Pain , Opioid-Related Disorders , Veterans , Humans , Analgesics, Opioid , Buprenorphine/therapeutic use , Chronic Pain/drug therapy , Chronic Pain/chemically induced , Opiate Substitution Treatment , Opioid-Related Disorders/drug therapy
2.
Proc Natl Acad Sci U S A ; 99(16): 10671-6, 2002 Aug 06.
Article in English | MEDLINE | ID: mdl-12149470

ABSTRACT

Huntington's disease (HD) is an untreatable neurological disorder caused by selective and progressive degeneration of the caudate nucleus and putamen of the basal ganglia. Although the etiology of HD pathology is not fully understood, the observed loss of neuronal cells is thought to occur primarily through apoptosis. Furthermore, there is evidence in HD that cell death is mediated through mitochondrial pathways, and mitochondrial deficits are commonly associated with HD. We have previously reported that treatment with tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, prevented neuropathology and associated behavioral deficits in the 3-nitropropionic acid rat model of HD. We therefore examined whether TUDCA would also be neuroprotective in a genetic mouse model of HD. Our results showed that systemically administered TUDCA led to a significant reduction in striatal neuropathology of the R6/2 transgenic HD mouse. Specifically, R6/2 mice began receiving TUDCA at 6 weeks of age and exhibited reduced striatal atrophy, decreased striatal apoptosis, as well as fewer and smaller size ubiquitinated neuronal intranuclear huntingtin inclusions. Moreover, locomotor and sensorimotor deficits were significantly improved in the TUDCA-treated mice. In conclusion, TUDCA is a nontoxic, endogenously produced hydrophilic bile acid that is neuroprotective in a transgenic mouse model of HD and, therefore, may provide a novel and effective treatment in patients with HD.


Subject(s)
Huntington Disease/drug therapy , Neuroprotective Agents/therapeutic use , Taurochenodeoxycholic Acid/therapeutic use , Animals , Apoptosis , Bile Acids and Salts/administration & dosage , Bile Acids and Salts/therapeutic use , Cell Nucleus/pathology , Corpus Striatum/cytology , Corpus Striatum/drug effects , Disease Models, Animal , Huntington Disease/pathology , Huntington Disease/physiopathology , Male , Mice , Mice, Transgenic , Motor Activity/drug effects , Nerve Degeneration/pathology , Nerve Degeneration/prevention & control , Neurons/cytology , Neurons/drug effects , Neuroprotective Agents/administration & dosage , Taurochenodeoxycholic Acid/administration & dosage
SELECTION OF CITATIONS
SEARCH DETAIL
...