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)

Two patients with typical Philadelphia chromosome positive chronic granulocytic leukaemia (CGL) developed an accelerated phase of the disease characterized by an increase white blood cell count and marked basophilia in the bone marrow and peripheral blood. Histamine levels were extremely high in both patients. Hyperhistaminaemia was manifested as wheezing, urticaria, diarrhoea, and pruritus in one patient and as peptic ulcer disease and peripheral oedema in both patients. In one case, gastric acid studies revealed a very high basal to stimulated ratio (BAO/MAO). Treatment with the investigational agent metiamide, an H2 receptor histamine antagonist, resulted in marked improvement in symptoms and reduction in gastric acid output. Extreme basophilia in CGL may be associated with hyperhistaminaemia, and manifestations of both the H1 and H2 type may occur.
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PMID:Basophilic chronic granulocytic leukaemia with hyperhistaminaemia. 26 9

Histamine metabolism was studied in 35 patients with polycythaemia vera (PV) at different stages of their disease and compared with controls and patients with secondary polycythaemia. In addition to blood and urinary histamine the main urinary metabolites of histamine, methylhistamine (MeHi) and 1-methyl-4-imidazoleacetic acid (MeImAA) were measured. In patients with active PV the excretion of MeHi and MeImAA was significantly higher than in controls and secondary polycythaemia, indicating an increased histamine formation. The MeImAA excretion was correlated to the blood histamine level, the degree of blood basophilia, the total white blood count and the spleen volume. The blood histamine level was significantly higher in PV patients compared with controls and secondary polycythaemia. No patients with secondary polycythaemia had an increased blood histamine level. With the bio-assay technique used in this study the urinary excretion of histamine in the PV patients was within the normal range. There was no correlation between the increased histamine formation and "histamine-related symptoms". Pruritus and duodenal ulcer occurred with a similar frequency in patients with and without increased MeImAA excretion. The similarity between the disturbance of the histamine metabolism in PV and that found by other authors in chronic myeloid leukaemia is pointed out.
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PMID:Histamine metabolism in polycythaemia vera. 117 64

Histamine is the key mediator producing itching, redness and chemosis in allergic conjunctivitis. Histamine levels in tears are increased ten-fold in patients with this allergic condition. Levocabastine is a newly synthesized histamine H1 antagonist which has been formulated as both eye drops and nasal spray. In well established assays of antihistamine activity, levocabastine was found to be the most potent antihistamine compound available, being 15,000 times more potent than chlorpheniramine. Ocular provocation studies in man have shown that levocabastine protects against the symptoms of allergen-induced conjunctivitis. Ophthalmological examinations, including slit lamp and ophthalmoscopy showed no adverse effects. Data from therapeutic studies are available for more than 1700 patients with allergic conjunctivitis treated for 2-16 weeks. One drop of levocabastine (0.5 mg/ml) per eye given two to four times daily provided significantly better symptom control than placebo, with good to excellent results in 71% of patients on levocabastine compared to 55% on placebo (p < 0.001). Levocabastine has a fast onset of action. In one study 94% of patients experienced symptom relief within 15 minutes after the first instillation. The effects observed with levocabastine were at least as good as those with ocular cromoglycate or oral terfenadine. The incidence of adverse experiences was not different from placebo. Levocabastine promises to be a valuable treatment for patients with allergic conjunctivitis.
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PMID:New trends in the treatment of allergic conjunctivitis. 136 81

Twenty-five febrile patients with a history of intravenous drug use who were receiving either vancomycin (15 patients) or teicoplanin (10 patients) as part of a multicenter, double-blind, randomized, clinical efficacy trial were enrolled, upon receipt of their first dose of antibiotic, into a study to evaluate the effect of 1 g of vancomycin and high-dose teicoplanin (30 mg/kg of body weight) on histamine release and the occurrence of "red man syndrome" (RMS). In addition, 10 healthy volunteer subjects (HVS) were randomized to receive either 1 g of vancomycin intravenously or a saline infusion in a double-blind, crossover design study. Patients and HVS were observed for the presence of erythema, flushing, pruritus, and hypotension during and for up to 1 h postinfusion by a blinded investigator. Histamine concentrations in plasma were measured at baseline and during and after drug infusion. No significant differences were noted in baseline temperature between patients (vancomycin recipients, 102.3 degrees F [39.1 degrees C]; teicoplanin recipients, 102.4 degrees F [39.1 degrees C]) or incidence of bacteremia (7 of 15 vancomycin recipients; 5 of 10 teicoplanin recipients). There were no significant differences in peak vancomycin concentrations in the sera of patients (40.8 micrograms/ml) and HVS (49.9 micrograms/ml). There were no reactions consistent with RMS in any patient who received teicoplanin (0 of 10); there was a significant difference in the occurrence of RMS in patients in comparison with that in HVS (0 of 15 patients, 9 of 10 HVS; P less than 0.001) who received vancomycin. The predominant reaction was erythema and pruritus. Histamine concentrations in plasma and the area under the histamine plasma concentration-time curve were highly variable within groups and were not statistically different between patients and HVS. The incidence of RMS secondary to vancomycin or teicoplanin in our patient population appears to be low and consistent with clinical observations. Similar to previous investigations, RMS secondary to vancomycin in HVS was high (90%). However, we found no relationship between the histamine concentration in plasma or the area under the plasma histamine concentration-time curve and the severity of RMS in HVS. The reason for the discrepancy of RMS in patients versus that in HVS in unknown, but it may be related to a blunted effect of glycopeptides to produce the reaction in the presence of infection or it may be specific to our patient population.
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PMID:Absence of "red man syndrome" in patients being treated with vancomycin or high-dose teicoplanin. 138 23

Since the majority of itching skin diseases are inflammatory or allergic, it has been assumed that release or activation of inflammatory mediators, stimulating the itch receptors, play an essential role in the pathophysiology of itch. In this review some of the possible mediators are discussed. Histamine induces itch upon intradermal injection, but urticaria is the only itching dermatosis which is significantly relieved by antihistamines. Serotonin is much weaker than histamine in provoking itch upon intradermal injection. Serotonin acting in synergism with prostaglandins may cause itch in polycythaemia vera. Neuropeptides release histamine from skin mast cells, but it remains to be determined whether neurogenic peptides are responsible for clinical pruritus. Prostaglandins enhance pruritus induced by intradermal histamine (and serotonin) but are weak pruritogens per se. Lymphocytes are present in many itching skin diseases and it could be assumed that lymphokines are involved in the pathogenesis of itch. Supporting this theory is the finding that ciclosporin A, an inhibitor of lymphokine production, reduces itch in atopic dermatitis. Central mechanisms are essentially unknown, but there are indications that opioid peptides might be involved in the central transmission of itch.
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PMID:Peripheral and central mediators of itch. 157 79

Histamine, which is stored mainly in mast cells and basophils, is a prominent contributor to allergic disease. Elevations in plasma or tissue histamine levels have been noted during anaphylaxis and experimental allergic responses of the skin, nose, and airways. Of the four cardinal signs of asthma (bronchospasm, edema, inflammation, and mucus secretion), histamine is capable of mediating the first two through its H1 receptor and mucus secretion through its H2 receptor. Of the five cardinal signs of allergic rhinitis (pruritus, mucosal edema, sneezing, mucus secretion, and late-phase inflammatory reactions), histamine is capable of mediating the first three through its H1 receptor. In the nose, mucus secretion can be reflexively mediated by H1 and possibly also by H2 receptors. In the skin the cardinal features of urticaria (vasodilation, vascular permeability, and pruritus) can be mediated by stimulation of the H1 receptor. In anaphylaxis histamine H1-receptor stimulation can mediate vascular permeability, smooth muscle contraction, and tachycardia, whereas H2-receptor stimulation can mediate mucus secretion. Stimulation of both receptors can mediate vasodilation and reduce peripheral vascular resistance. Thus although histamine is only one of many mediators of allergic disease, it plays a primary role in allergic rhinitis, urticaria, anaphylaxis, and to a lesser degree, asthma.
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PMID:The role of histamine in allergic diseases. 169 87

Psychophysical measurements of itch and itchy skin ("alloknesis"--itch produced by innocuous mechanical stimulation) were obtained in human volunteers following intracutaneous or subcutaneous injections of histamine or papain into the volar forearm. Histamine and papain were given in doses of 0.1, 1, or 10 micrograms in 10 microliters of saline. The effects of the depth of injection and of skin temperature on the latency, magnitude, and duration of itch were examined. Also, dose-response functions were obtained for the area of alloknesis produced by intracutaneous injections of histamine. Finally, the neural mechanisms underlying the spread of alloknesis were investigated via local anesthesia of the skin. Intracutaneous and subcutaneous injections of histamine, but not papain, produced a sensation of itch without pain. The latency of itch was shorter after an intracutanous than after a subcutaneous injection of histamine. The mean latencies of itch produced by a 1-microgram dose were 9.5 and 23.0 sec for intracutaneous and subcutaneous injections, respectively. No differences were observed in the magnitude or duration of itch. Similarly, the latency of itch was increased when the skin temperature at injection site was lowered to 15 degrees C, whereas the magnitude and duration of itch were unaffected. Intracutaneous and subcutaneous injections of histamine produced similar areas of alloknesis. However, the magnitude and duration of alloknesis were dependent on dose. The mean maximum areas of alloknesis produced by intracutaneous injections of 0.1, 1, and 10 micrograms of histamine were 28.3, 47.2, and 43.8 cm2, respectively. Alloknesis was present at 2 min after injection, increased to a maximum area without 10 min, and then gradually decreased during the next 25-40 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Psychophysical studies of the itch sensation and itchy skin ("alloknesis") produced by intracutaneous injection of histamine. 176 23

Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm. Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects. Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.
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PMID:Histamine-induced coronary artery spasm: the concept of allergic angina. 179 97

1. The aim of this investigation was to study the peripheral neural mechanisms of the C-fiber-mediated modalities of burning pain and itch by the use of microneurography of human unmyelinated afferents. 2. Sixteen stable recordings of single C-fibers and 6 multiunit recordings were obtained from the superficial radial nerves of volunteers. All units were excited by stimulating their receptive fields with von Frey bristles (range 10-600 mN), and all but four units were also driven by radiant heat stimulation. 3. Histamine was iontophoretically applied to the receptive fields of these units for 20 or 30 s and was found to provoke itching sensations lasting several minutes, together with wheal and flare responses. Subsequently a solution containing 20 or 30% mustard oil was applied to the receptive field of the respective unit, which provoked a sensation of burning pain. 4. One-half of the units were excited by histamine, and the median discharge rates derived from interspike intervals ranged from approximately 0.1 to 0.8 Hz. Mustard oil-induced activity was observed in all histamine-sensitive units and also in three single units and in one multiunit recording that revealed no histamine response. Median interval-derived discharge rates ranged from 0.2 to 1.2 Hz. 5. Analysis of the interspike interval distribution and of the autocorrelation function derived from the chemically induced discharges of single units provided no evidence for an encoding of itch and burning pain in different discharge patterns of units responding to histamine and to mustard oil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Discharge patterns of human C-fibers induced by itching and burning stimuli. 191 73

Histamine is known to be a classical inducer of pruritus. In atopic eczema, itch is a prominent feature (regarded by some even as a 'primary lesion'!). One of the most potent chemical mediators of itch is histamine. Histamine, together with other mediators may play a role in the pathophysiology of atopic eczema: the increased release of histamine from basophil leucocytes of atopic patients has been described, as well as elevated histamine levels in plasma and skin during acute exacerbations of eczematous lesions. Therefore, application of H1 antagonists seems to be a rational regime in the symptomatic treatment of atopic eczema. Nevertheless, some controversy exists regarding the clinical efficacy of orally applied H1 antagonists in this disease, especially with regard to the newer non-sedating compounds such as terfenadine, astemizole, loratadine and cetirizine. Review of the literature shows that there are studies demonstrating a clear-cut antipruritic effect of non-sedating H1 antagonists. Thus the sedative action does not seem necessarily to be connected with therapeutic efficacy in treating itch in atopic eczema. Newer studies show that cetirizine exerts an additional inhibitory effect on eosinophils. This may broaden the therapeutic spectrum of this H1 antagonist in diseases with eosinophil involvement.
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PMID:Histamine, antihistamines and atopic eczema. 198 Aug 56


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