Pharmacologic advances in the systemic treatment of itch

Summey, Brett T.; Yosipovitch, Gil

doi:10.1111/j.1529-8019.2005.00035.x

Cited by 50 publications

(31 citation statements)

References 42 publications

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“…If these factors play a significant role, the anxiolytic effect of mirtazapine by 5-HT 2 antagonism and the antidepressant effect by 5-HT 1A stimulation might reduce PONV. Third, mirtazapine may inhibit neuronal transmission by decreasing neurotransmitter release [18]. Fourth, there is cross-talk between voltage-gated Ca 2+ channels and 5-HT 3 receptors [19].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of mirtazapine in preventing intrathecalmorphine‐induced nausea and vomiting after orthopaedic surgery*

Chang

Sheen

2010

Anaesthesia

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SummaryNausea and vomiting are frequent complications of intrathecal morphine. In this randomised, double-blind trial, we tested the efficacy of mirtazapine, an antidepressant that blocks receptors associated with vomiting, on the incidence of nausea and vomiting after intrathecal morphine. One hundred patients receiving spinal anaesthesia for lower limb surgery were assigned equally to take either an orally disintegrating form of 30 mg mirtazapine or matching placebo 1 h before surgery. Spinal anaesthesia was performed by injection of 15 mg isobaric bupivacaine 0.5% along with 0.2 mg preservative-free morphine. Nausea and vomiting were evaluated 3, 6, 12, 18 and 24 h after intrathecal morphine administration. The incidence of nausea and vomiting was significantly lower in patients receiving mirtazapine compared with placebo (26.5% vs 56.3%, respectively; p = 0.005). The mean (SD) onset time of postoperative nausea and vomiting was significantly delayed in mirtazapine patients: 9.4 (2.5) vs 5.2 (1.8) h, respectively; p < 0.0001. The severity of nausea and vomiting was also decreased after mirtazapine at the 3-6 h and 6-12 h periods. Our data indicate that pre-operative mirtazapine decreases the incidence, delays the onset and reduces the severity of nausea and vomiting induced by intrathecal morphine in patients undergoing spinal anaesthesia. A single dose of intrathecal morphine is often administered to patients undergoing major orthopaedic procedures to provide sustained postoperative analgesia. Postoperative nausea and vomiting (PONV) occurs frequently, with a reported incidence of up to 74% and lasting up to 24 h [1]. Serotonin (5-HT 3 ) receptor antagonists have been used as anti-emetics to prevent or to treat nausea and vomiting induced by intrathecal morphine [2][3][4][5][6]. Mirtazapine is a new antidepressant that selectively blocks postsynaptic 5-HT 2 and 5-HT 3 receptors [7]. As it blocks receptors associated with nausea and vomiting, mirtazapine had been shown to treat severe vomiting during pregnancy [8] and to treat cancer patients with pain, nausea and a variety of distressing symptoms [9,10]. Its anti-emetic effect has also been reported after laparoscopy surgery [11] and gastric bypass [12]. Its effect on the prevention of intrathecal morphine-induced PONV has not yet undergone evaluation. We therefore hypothesised that prophylactic mirtazapine would reduce the incidence and delay the onset of intrathecal morphine-induced PONV in patients undergoing orthopaedic surgery. MethodsThe protocol was approved by the Clinical Research Ethics

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Section: Discussionmentioning

confidence: 99%

Efficacy of mirtazapine in preventing intrathecalmorphine‐induced nausea and vomiting after orthopaedic surgery*

Chang

Sheen

2010

Anaesthesia

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“…The H1 receptor is the most extensively histamine receptor studied. Indeed, H1 receptor blockers have an established and valued place in the treatment of itching of allergic and non-allergic origin (Skidgel et al, 2011).However, intriguing data on the H3 receptor seem to contradict the aforementioned histamine-induced itch pathway (Summey and Yosipovitch, 2005); antagonists such as thioperamide and AQ0145 were found to increase significantly the incidence of scratching behaviour in mice (Sugimoto et al, 2004). It is possible that these histamine H3 receptor antagonists block the modulatory role of the presynaptic H3 receptor, thus favouring the release of neuropeptides from sensory endings (Cannon et al, 2007).…”

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confidence: 99%

The role of histamine in neurogenic inflammation

Rosa

Fantozzi

2013

British J Pharmacology

170

138

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The term 'neurogenic inflammation' has been adopted to describe the local release of inflammatory mediators, such as substance P and calcitonin gene-related peptide, from neurons. Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established. The aim of this review is to summarize the most recent findings on the role of histamine in neurogenic inflammation, with particular regard to nociceptive pain, as well as neurogenic inflammation in the skin, airways and bladder. LINKED ARTICLESThis article is part of a themed issue on Histamine Pharmacology Update. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2013.170.issue-1 Abbreviations CGRP, calcitonin gene-related peptide; ERs, oestrogen receptors; GERD, gastro-oesophageal reflux disease; HDC, histidine decarboxylase; IC, interstitial cystitis; PBS, painful bladder syndrome; SP, substance P; VIP, vasoactive intestinal peptide IntroductionThe term 'neurogenic inflammation' describes the local release of inflammatory mediators, such as substance P (SP) and calcitonin gene-related peptide (CGRP), from afferent neurons. The initial evidence for neurogenic vasodilatation in response to noxious stimuli was obtained in the skin of humans and other mammals (Schmelz and Petersen, 2001), but now it is recognized that neurogenic inflammation also occurs in visceral organs. The inflammatory response evoked by the activation of the sensory nerve fibres, which includes local vasodilatation, plasma extravasation, leukocyte and platelet adhesion, and mast cell degranulation, is brought about by neuropeptides released from the peripheral endings of sensory neurons upon stimulation of the primary sensory terminals. Both SP in neurons and histamine in mast cells have a dual mediator role in neurogenic inflammation (Figure 1). In fact, as demonstrated by Foreman and Jordan (1984), injury causes activation of sensory nerve endings either directly or through the release of histamine from the adjacent mast cells. The action potential generated travels orthodromically to the dorsal horn of the spinal cord and spreads to other branches of the same neurons, which will then release SP from their terminals or varicosities. The released SP, as well as contributing itself to local vasodilatation, induces histamine release from the adjacent mast cells, which produces flare and further activates other sensory nerve endings (Foreman et al., 1983).Neutrophils, whose responsiveness to SP has been repeatedly demonstrated, contribute to the inflammatory soup following neurogenic inflammation. In fact, neutrophils express the SP receptors NK 1, NK2 and NK3, and when stimulated with SP induce the expression of COX-2 and PGE2 release in the nanomolar range (Gallicchio et al., 2008;. Furthermore, SP at micromolar concentrations primes neutrophils, thus en...

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“…Antidepressants such as sertraline, mirtazapine and paroxetine have been demonstrated to have antipruritic efficacy in the clinic. 62,63 In addition, severe neuropathic itch associated with herpes zoster resolved after epidural treatment with concomitant clonidine and bupivacaine. 64 Unlike in neuropathic pain, μ opioids should be avoided in the treatment of pruritus because of their itch-inducing side effect.…”

Section: Treatment Of Neuropathic Itchmentioning

confidence: 99%

Disease mechanisms in neuropathic itch

2008

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Itch, also known as pruritus, is an unpleasant cutaneous sensation that provokes the desire to scratch. Itch is a common symptom of inflammatory skin disorders, but it can also occur in neurological diseases associated with injury to nervous tissue, in the absence of any skin disease and without any notable physiological stimuli in the periphery. This 'neuropathic' type of itch occurs either in combination with neuropathic pain or independently and is thought to be underdiagnosed. In this Review, we describe the physiological characteristics of specific neuronal systems in the PNS and CNS that transmit and process pruriceptive information, and we consider pathological changes that occur in these systems after nerve lesions. We then introduce a classification system for itch and highlight the similarities and differences between neuropathic itch and neuropathic pain. A summary of neuropathic syndromes in the PNS and CNS that are associated with itch is presented. Finally, we propose appropriate treatment strategies for neuropathic itch, in view of the fact that this condition has different mechanisms of itch generation to other types of itch and consequently requires different therapies.

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Pharmacologic advances in the systemic treatment of itch

Cited by 50 publications

References 42 publications

Efficacy of mirtazapine in preventing intrathecalmorphine‐induced nausea and vomiting after orthopaedic surgery*

Efficacy of mirtazapine in preventing intrathecalmorphine‐induced nausea and vomiting after orthopaedic surgery*

The role of histamine in neurogenic inflammation

Disease mechanisms in neuropathic itch

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