Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of naloxone in reducing the incidence of side effects after intrathecal injection of morphine and the effects of maternal naloxone administration on the condition of the newborn were evaluated in 40 patients. Patients in labor were given a 1-mg intrathecal injection of morphine and, 1 hr later, either a 0.4-mg bolus of naloxone, followed by a 0.4-0.6 mg/hr intravenous infusion of naloxone, or an intravenous bolus of saline, followed by an intravenous infusion of saline. Intrathecal morphine provided at least 50% pain relief in 78% of patients given naloxone, and in 82% given saline. Intravenous naloxone significantly decreased the incidence of pruritus during labor and delivery. There was no significant decrease in the incidence of nausea, vomiting, somnolence, dizziness, or urinary retention in patients given naloxone. Despite placental transfer of naloxone, neonatal outcome was not adversely affected. For both groups, maternal beta-endorphin levels decreased significantly with the onset of analgesia and returned to control levels at delivery. We conclude that intravenous infusion of naloxone reduced pruritus after intrathecal injection of 1 mg of morphine for labor pain without lessening analgesia or adversely affecting maternal or neonatal status.
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PMID:The effects of naloxone associated with the intrathecal use of morphine in labor. 316 Feb 59

The effect of various opioid or putative neurotransmitter peptides on histamine-induced itch and flare responses was studied in humans after intradermal injection. Significant enhancement of the histamine responses was induced by the stable methionine-enkephalin analogue FK 33-824, beta-endorphin and morphine. The putative neurotransmitters substance P and vasoactive intestinal polypeptide (VIP)--which moreover are potent histamine liberators--had no enhancing effect. The potentiation induced by FK 33-824 was induced neither by local pretreatment with Compound 48/80 to deplete the local stores of mast-cell-bound histamine, nor by oral pretreatment with indomethacin to inhibit prostaglandin formation in the skin. Thus, the enhancement did not seem to be due to histamine release or to prostaglandin formation and the mechanism of the effect remains to be shown. The specific morphine antagonist naloxone did not inhibit the potentiation by FK 33-824, which might indicate that ordinary opiate receptors were not involved. The results support the idea that pain and itch are qualitatively separate processes and suggest possible mechanisms of morphine-induced pruritus. The findings are of particular interest in view of recent reports on the presence of methionine-enkephalin in Merkel cells.
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PMID:Potentiation of histamine-induced itch and flare responses in human skin by the enkephalin analogue FK-33-824, beta-endorphin and morphine. 618 98

Atopic dermatitis (AD) is a pruritic cutaneous inflammatory condition. As pruritus and pain are very close symptoms, we determined the beta-endorphin serum concentrations in 21 atopic children with pruritus (group A) and 20 children with healed AD without pruritus (group B). Twenty-five healthy school children were the control group. The beta-endorphin serum concentrations (14.95 +/- 2.75 pmol/l) in group A were statistically (P < 0.001) elevated in our patients compared to controls (8.85 +/- 2.39 pmol/l) whereas these in group B were not elevated (9.4 +/- 2.46 pmol/l). We suggest that the elevated beta-endorphin concentrations in atopic patients with pruritus confirm the hypothesis that there is an increased activity of their opioid system and that an opioid antagonist might block itching which is their major clinical symptom.
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PMID:Raised beta-endorphin serum levels in children with atopic dermatitis and pruritus. 784 Nov 55

Serum beta-endorphin was quantified by radioimmunoassay in 71 patients with psoriasis vulgaris, other chronic inflammatory skin diseases with T-cell infiltrates [atopic dermatitis (n = 25), and systemic sclerosis (n = 34)], and 100 healthy subjects. The neuropeptide was found to be markedly (P < 0.001) increased in patients with psoriasis (14.4 pg/ml), atopic dermatitis (9.2 pg/ml) and systemic sclerosis (9.8 pg/ml) compared with normal controls (6.1 pg/ml). The highest values of beta-endorphin were found in patients with actively spreading plaque psoriasis (17.3 pg/ml), whereas lesion-free patients showed a reduction in neuropeptide concentration (10.2 pg/ml). The levels were much higher in patients with widespread psoriatic lesions (> 60% body surface; 16.2 pg/ml), which lasted longer than 3 months (15.8 pg/ml), whereas neither the presence of stress nor itching correlated with the serum peptide concentration. Our data suggest that beta-endorphin is produced in psoriatic lesions by inflammatory cells, rather than the increased levels being the result of activation of the pituitary-adrenal axis by chronic stress. The generation of neuropeptide in psoriatic lesions and its antinociceptive effect on the peripheral sensory nerves might explain why pruritus is a relatively rare phenomenon in psoriasis.
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PMID:Increased concentration of beta-endorphin in sera of patients with psoriasis and other inflammatory dermatoses. 791 92

Adrenocortical adenoma, nodular hyperplasia, or carcinoma was diagnosed in 50 ferrets. Thirty-five (70%) ferrets were female and 15 (30%) were male. The mean age at which clinical signs were first noticed was 3.4 years (range, 1 to 7 years). Clinical signs included large vulva (n = 31; 89% of females), alopecia (n = 43; 86%), pruritus (n = 20; 40%), and increased consumption of water and increased urine output (n = 4; 8%). A mass was palpated at the cranial pole of the kidney during physical examination of 17 (34%) ferrets. Ultrasonography, performed on 39 of 50 ferrets, revealed a unilateral adrenal gland mass in 19 (49%). Four ferrets were anemic, and 2 ferrets were thrombocytopenic. Baseline plasma concentrations of cortisol and corticosterone were within or below the reference range in all 17 ferrets tested, whereas baseline plasma estradiol concentrations were high in 4 of the 11 ferrets (36%) tested. AFter adrenocorticotropic hormone (ACTH) administration, only 1 ferret had a slightly exaggerated response on the basis of plasma cortisol concentrations, and all 17 had normal responses on the basis of plasma corticosterone concentrations. There was little or no increase in plasma estradiol concentrations after ACTH administration. Of the 50 ferrets, 39 were treated by adrenalectomy. Unilateral adrenalectomy was performed in 34 ferrets in which 1 adrenal gland was large, whereas subtotal bilateral adrenalectomy was performed in 5 ferrets with bilateral adrenal disease. Five ferrets died in the immediate postoperative period, and follow-up information was available for the remaining 34, 1 to 34 months after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperadrenocorticism associated with adrenocortical tumor or nodular hyperplasia of the adrenal gland in ferrets: 50 cases (1987-1991). 840 89

Met-enkephalin plasma levels were measured in 21 hemodialysis patients with or without pruritus. The mean value was significantly increased in the total of the patients compared with that in ten healthy subjects. There was, however no correlation between met-enkephalin levels and the degree of pruritus. The findings suggest that the opioid system may be activated in this condition, although the relevance of this endogenous opioid peptide to pruritus remains to be determined.
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PMID:Increased met-enkephalin plasma levels in hemodialysis patients with or without pruritus. 859 68

Many skin disorders, such as atopic dermatitis and psoriasis, worsen during stress and are associated with increased numbers and activation of mast cells which release vasoactive, nociceptive, and proinflammatory mediators. Nontraumatic acute psychological stress by immobilization has been shown to induce mast cell degranulation in the rat dura and colon. Moreover, intradermal injection of corticotropin-releasing hormone (CRH) or its analogue urocortin (10(-5)-10(-7) M) induced skin mast cell degranulation and increased vascular permeability. Here, we investigated the effect of acute immobilization stress on skin mast cell degranulation by light microscopy and electron microscopy. Immobilization for 30 min resulted (P < 0.05) in degranulation of 40.7 +/- 9.1% of skin mast cells compared to 22.2 +/- 7.3% in controls killed by CO(2) or 17.8 +/- 2.4% in controls killed by pentobarbital. Pretreatment intraperitoneally (ip) with antiserum to CRH for 60 min prior to stress reduced (P < 0.05) skin mast cell degranulation to 21.0 +/- 3. 3%. Pretreatment with the neurotensin (NT) receptor antagonist SR48692 reduced (P < 0.05) mast cell degranulation to 12.5 +/- 3.4%, which was significantly (P < 0.05) below control levels. In animals treated neonatally with capsaicin to deplete their sensory neurons of their neuropeptides, such as substance P (SP), mast cell degranulation due to immobilization stress was reduced to about 15%. This is the first time that stress has been shown to trigger skin mast cell degranulation, an action not only dependent on CRH, but apparently also involving NT and SP. These findings may have implications for the pathophysiology and possible therapy of neuroinflammatory skin disorders such as atopic dermatitis, neurogenic pruritus, or psoriasis, which are induced or exacerbated by stress.
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PMID:Acute immobilization stress triggers skin mast cell degranulation via corticotropin releasing hormone, neurotensin, and substance P: A link to neurogenic skin disorders. 1046 24

There is increasing evidence that neuropeptides such as a substance P, neurotrophins or beta-endorphin, an endogenous agonist for mu-opioid receptor, are involved in the pathogenesis of atopic dermatitis in which mental stress and scratching deteriorate the disease. mu-Opioid receptor, a G-protein-coupled receptor, can be downregulated and internalized by agonists and other factors in vitro. In this study, we investigated the regulation of mu-opioid receptor and nerve endings in atopic dermatitis patients. Skin biopsies from atopic dermatitis patients revealed a significant downregulation of mu-opiate receptor expression in epidermis of atopic dermatitis. Permeabilization of the skin showed that the receptor in keratinocytes from atopic dermatitis is internalized. The mRNA expression pattern of the mu-opiate receptor is different in epidermis taken from patients with chronic atopic dermatitis compared to normal skin. In atopic dermatitis, the mRNA is concentrated in the subcorneal layers of the epidermis and in normal skin in the suprabasal layers. Staining of the nerve endings using protein gene product 9.5 shows a different pattern of epidermal nerve endings in normal skin compared to atopic dermatitis. In normal skin, the epidermal nerve endings are rather thick. However, in atopic dermatitis, the epidermal nerve endings are thin and run straight through the epidermis. Based on these observations and combining the 'intensity' and 'pattern' hypothesis, we propose a new theory especially for histamine-unrelated, peripheral induction of chronic pruritus. We suggest that 'itch' is elicited in the epidermal unmyelinated nerve C-fibers and 'pain' in the dermal unmyelinated nerve fibers. The downregulation of the opioid receptor in the epidermis contributes to the chronic itching. We call this new hypothesis the 'layer hypothesis'.
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PMID:Changes of epidermal mu-opiate receptor expression and nerve endings in chronic atopic dermatitis. 1572 90

The micro-opioid (beta-endorphin/micro-opioid receptor) and kappa-opioid (dynorphin A (DynA)/kappa-opioid receptor) systems play pivotal roles in the modulation of pruritus in the central nervous system. The micro-opioid system has also been identified in human epidermis, raising the possibility that the system controls the peripheral itch. However, the precise distribution of the kappa-opioid system has not yet been clarified in human epidermis. To address this issue, reverse transcription-PCR and immunohistochemical analyses were performed on cultured keratinocytes and normal skins from humans. The analyses revealed that epidermal keratinocytes express kappa-opioid receptor and its ligands, DynA (1-17) and DynA (1-8). Moreover, expression for micro- and kappa-opioid systems was examined immunohistochemically in skin biopsies from healthy volunteers and patients with atopic dermatitis (AD) before and after psoralen-ultraviolet A (PUVA) therapy. Our expression analyses showed that only the kappa-opioid system, not the micro-opioid system, was downregulated in the epidermis of AD patients. The downregulation of the micro-opioid system and the restoration of the kappa-opioid system by PUVA therapy were observed in the AD patients, concomitant with a decrease of VAS (visual analogue scale) scores. These results suggest epidermal opioid systems are associated with the modulation of pruritus in AD. This new finding may help us to understand the control mechanism of peripheral itch.
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PMID:Possible roles of epidermal opioid systems in pruritus of atopic dermatitis. 1761 80

Perceived stress has long been allied with disturbances of the dynamic equilibrium established between the nervous, endocrine and immune systems, thus triggering or aggravating disease manifestation. Several common skin diseases are now acknowledged to be worsened by psychological stress, particularly immunodermatoses such as atopic dermatitis, psoriasis, seborrheic eczema, prurigo nodularis, lichen planus, chronic urticaria, alopecia areata and pruritus sine materia. Itch (pruritus) is perhaps the most common symptom associated with a majority of these inflammatory skin diseases, and acute as well as chronic stress perceptions are recognized to trigger or enhance pruritus. A wealth of mediators released systemically or locally in the skin in response to stress increase sensory innervation, upregulate the production of other pruritogenic agents, perpetuate (neurogenic) inflammation and lower the itch threshold. In the present review, we explore recent frontiers in both stress and pruritus research and portray the perpetuation of chronic skin inflammation and itch as a neuroendocrine-immune 'misalliance'. We argue that key candidate molecules of the stress response with strong pruritogenic potential, such as nerve growth factor, corticotropin-releasing hormone and substance P, and mast cells, which may be considered as 'central cellular switchboards of pruritogenic inflammation', need to be further explored systematically in order to develop more effective therapeutic combination strategies for itch management in chronic, stress-vulnerable inflammatory skin diseases.
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PMID:From the brain-skin connection: the neuroendocrine-immune misalliance of stress and itch. 1770 57


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