Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Topical capsaicin has been introduced in the U.S. and Canada as a cream indicated for temporary relief of neuralgia following episodes of herpes zoster infections and in the treatment of diabetic neuropathy. Although capsaicin is clinically used as an external analgesic for temporary relief of neuralgia, it has also been widely used as a research tool to study peripheral pain. Capsaicin apparently works to release substance P from sensory nerve fibers and after repeated applications, depletes neurons of substance P. Clinical investigations of topical capsaicin include trials in chronic pain syndromes such as postherpetic neuralgia, postmastectomy neuroma, reflex sympathetic dystrophy syndrome, diabetic neuropathy, rheumatoid arthritis, psoriasis, hemodialysis-associated itching, and vulvar vestibulitis. In addition, therapeutic benefits of capsaicin cream on apocrine chromhidrosis have been described. Further clinical studies are warranted in several of these conditions to establish the efficacy of topical capsaicin. Serious or unexpected adverse reactions from clinical use have not been reported to date. Considering the paucity of safe and effective treatments for the conditions mentioned above, capsaicin cream appears to warrant further clinical investigations to establish its efficacy in a variety of chronic pain syndromes.
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PMID:Topical capsaicin in dermatologic and peripheral pain disorders. 165 16

A 31-year-old woman with intractable reflex sympathetic dystrophy experienced nearly complete, though temporary, resolution of pain following 3 weeks of topical capsaicin. We propose that capsaicin may be a useful treatment for reflex sympathetic dystrophy, either by depleting substance P from primary afferent neurons that mediate allodynia, or by modulating sympathetic efferent activity.
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PMID:Treatment of reflex sympathetic dystrophy with topical capsaicin. Case report. 170 Dec 33

We treated a 65 year-old man with severe facial pain after extended maxillectomy due to carcinoma of maxillar sinus. He had been suffering from pain at rest, on mastication, or at treatment of surgical wound. Various kinds of analgesics had been tried, but his pain did not disappear. At 17 weeks after the operation, he came to our pain clinic. Because his pain was thought to be due to reflex sympathetic dystrophy (RSD), stellate ganglion blocks (SGB) were performed. After 5 administrations of SGB, pain was reduced markedly but the pain at treatment of wound persisted. We thought that persistent pain would need trigeminal nerve block. Then Gasserian ganglion block was performed directly through an open wound after the operation. After the Gasserian ganglion block, the pain was diminished remarkably. He could tolerate procedures for facial prosthesis. Pain control after the operation in this patient was very efficient to improve his quality of life. Serum concentrations of catecholamines, serotonin and substance P were measured. The levels of norepinephrine and serotonin are related to the mechanism of pain as seen in this patient.
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PMID:[Management of severe pain after extended maxillectomy in a patient with carcinoma of the maxillary sinus]. 886 30

Concepts related to the pathophysiology of reflex sympathetic dystrophy syndrome (RSDS) are changing. Although sympathetic influences are still viewed as the most likely mechanism underlying the development and/or perpetuation of RSDS, these influences are no longer ascribed to an increase in sympathetic tone. Rather, the most likely mechanism may be increased sensitivity to catecholamines due to sympathetic denervation with an increase in the number and/or sensitivity of peripheral axonal adrenoceptors. Several other pathophysiological mechanisms have been suggested, including neurogenic inflammation with the release of neuropeptides by primary nociceptive afferents and sympathetic efferents. These neuromediators, particularly substance P, calcitonin gene-related peptide, and neuropeptide Y (NPY), may play a pivotal role in the genesis of pain in RSDS. They induce an inflammatory response (cutaneous erythema and edema) and lower the pain threshold. Neurogenic inflammation at the site of the lesion with neuromediator accumulation or depletion probably contributes to the pathophysiology of RSDS. However, no single neuromediator has been proved responsible, and other hypotheses continue to arouse interest.
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PMID:Reflex sympathetic dystrophy syndrome and neuromediators. 1263 12