Морфологическая, иммуногистохимическая и ультраструктурная характеристика синдрома хронической тазовой боли при наружном генитальном эндометриозе
Observational
OA: closed
CC0
AI-generated summary
This study of 60 external genital endometriosis cases identified inflammation-induced nerve irritation as a pain mechanism, revealing a correlation between TRPV1 receptor expression and pain intensity that suggests pharmacological targeting for treatment.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
The results of studying 60 cases external genital endometriosis have shown that one of mechanisms of pain occurrence is caused by inflammation at which there is a direct irritation of nerve ending by inflammation mediators leading to ultrastructural changes in nervous fibres and development of pain syndrome. Direct correlation dependence between expressiveness of vanilloid type 1 receptors in ectopic endometrium and the intensity of pain syndrome that opens prospects for pharmacological block TRPV1 is revealed and can be pathogenetic treatment of pain syndrome at endometriosis.
My notes (saved in your browser only)
Condition tags
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.
Source provenance
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0
· commercial use OK