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)

Chronic urticaria defined as repeated or daily eruptions of wheals within a week over a period of at least 1 1/2 months is a frustrating problem not only for the patient but also for the physician. Since a cause will seldom be identified, therapy is symptomatic. In this study the effect of fexofenadine the active metabolite of terfenadine on pruritus, wheal formation and subjective feedbacks has been investigated in 21 patients with chronic urticaria. The study was double-blind, placebo-controlled designed. Following a 1-week washout period all study subjects received fexofenadine 180 mg OD for 3 weeks; thereafter the subjects were randomized for another 3 weeks in a placebo and fexofenadine arm. This study showed that fexofenadine had a beneficial effect on urticaria, particularly pruritus, and the patient-reported symptoms. Reports on side effects were non characteristic and not different between fexofenadine and placebo. Prolongation of QTc intervals or other cardiac side effects have not been observed. Fexofenadine 180 mg is a new antihistamine that is effective in the treatment of chronic urticaria and that has a profile of side effects similar to placebo.
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PMID:[Chronic idiopathic urticaria: effectiveness of fexofenadine. A double-blind, placebo controlled study with 21 patients]. 1201 63

Chronic idiopathic urticaria (CIU), characterized by the appearance of itchy wheals of unknown etiology, can be extremely debilitating and can significantly reduce a patient's quality of life (QOL). Fexofenadine, a non-sedating, H1-receptor selective, long-acting antihistamine, is licensed worldwide for the treatment of CIU. A number of dose-ranging studies have evaluated the efficacy and safety of fexofenadine for the the treatment of CIU. In two similar North American studies, patients received either fexofenadine HCI (20, 60, 120, or 240 mg bid) or placebo. All four doses of fexofendine were statistically superior to placebo at reducing pruritus and reducing the number of wheals (P < or = 0.0238). A dose-finding study undertaken in Japanese patients confirmed that fexofenadine HCI (60 mg and 120 mg bid) is an effective treatment for CIU. A similar dose response was shown in all three studies when the results were compared. Furthermore, health outcome analyses of the North American studies indicated that fexofenadine HCI 60 mg bid significantly improved patient's QOL. In these studies, fexofenadine had a consistently comparable safety profile to placebo, with no dose-related trends in the incidence of adverse events. In conclusion, fexofenadine is an effective and well-tolerated treatment for CIU, with a wide therapeutic window. Importantly, the lack of ethnic differences between the studies from North America and Asia indicate that the efficacy and safety of fexofenadine demonstrated in these studies are cross-culturally applicable.
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PMID:Review of fexofenadine in the treatment of chronic idiopathic urticaria. 1239 Feb

Allergen specific nasal challenge (ASNC) is an optimal model to study the pathophysiological mechanisms sustaining allergic inflammation, particularly the cytokine pattern. Antihistamines have been accepted as a highly effective therapy for allergic rhinitis. The aim of this double blind, randomised, placebo controlled study was the evaluation of symptoms and cytokines, during the early phase, after a single dose of mizolastine (10 mg), fexofenadine (120 mg) or placebo, using the model of ASNC. A total of 30 patients with allergic rhinitis underwent nasal challenge 6 hours after treatment. The following parameters were evaluated 30 minutes after ASNC (i.e. early phase): nasal symptoms (rhinorrhea, itching, sneezing, obstruction), and cytokine pattern, including IL1, IL6, and TNFalpha. Mizolastine was associated with early phase reduction of: i) clinical symptoms (p < 0.03), ii) cyotkine levels of IL1 (p = 0.003), IL6 (p < 0.007), and TNF_ (p < 0.003) in comparison with placebo group. Fexofenadine significantly inhibited IL6 (p < 0.004) and TNFalpha (p < 0.004) levels in comparison with placebo. The present findings demonstrate that mizolastine exerts a significant effect on early phase events, reducing symptoms and pro-inflammatory cytokines. Fexofenadine reduces TNFalpha and IL6 levels only. These effects appear to be clinical relevant for mizolastine.
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PMID:Mizolastine and fexofenadine modulate cytokine pattern after nasal allergen challenge. 1518 Mar 56

Fexofenadine, a histamine H1-receptor antagonist, is approved for the treatment of pruritus associated with atopic dermatitis. The effects of fexofenadine on scratching behaviour, and plasma levels of histamine and eotaxin were assessed in a new model of atopic dermatitis. Mice fed a diet low in Mg2+ and Zn2+ (special diet S) were compared with mice on a normal diet (N) or diet S plus fexofenadine HCl for weeks 0-10 (S + F(0-10)), 0-5 (S + F(0-5)) or 6 - 10 (S + F(6-10)) (seven mice per group). Compared with group N, group S mice showed significantly greater scratching frequency, and plasma histamine and eotaxin concentrations; these three variables were significantly lower in group S + F(0-10) than in group S. Scratching frequency increased when fexofenadine was discontinued. Fexofenadine significantly reduced mast cell and eosinophil numbers. Histamine may be important in the pathological changes seen in this model of atopic dermatitis, suggesting that it might aid future development of antihistamines for the treatment of atopic dermatitis.
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PMID:The effect of fexofenadine on pruritus in a mouse model (HR-ADf) of atopic dermatitis. 1713 78

Many medicines exist which can cause pruritus (itching) as "serious adverse events." Many severe pruritic conditions respond poorly to histamine H1 receptor antagonists; there is no generally accepted antipruritic treatment. Recently described histamine H4 receptors are expressed in haematopoietic cells and have been linked to the pathology of allergy and asthma. We previously reported their expression in human dermal fibroblasts; in this study we have investigated H4 receptor expression in human epidermal tissue and found it to be greater in keratinocytes in the epidermal upper layer than in the lower layer. We have also investigated the effect of histamine H4 receptor antagonists on histamine H1 receptor antagonist-resistant pruritus using a mouse model. Scratching behavior was induced by histamine (300 nmol) or substance P (100 nmol) injected intradermally into the rostral part of the back of each mouse. Fexofenadine, a histamine H1 receptor antagonist, reduced scratching induced by histamine but not by substance P, whereas JNJ7777120, a histamine H4 receptor antagonist, significantly reduced both histamine- and substance P-induced scratching. These results suggest that H4 receptor antagonists may be useful for treatment of H1 receptor antagonist-resistant pruritus.
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PMID:Expression of histamine H4 receptor in human epidermal tissues and attenuation of experimental pruritus using H4 receptor antagonist. 1965 66

Chronic idiopathic urticaria (CIU) is a serious disorder that can greatly compromise quality of life. While H1 antihistamines are the accepted first-line treatment for CIU, older generations of these agents (e.g., hydroxyzine, diphenhydramine) are associated with anticholinergic and CNS effects, such as drowsiness and sedation, that can pose risks to patients, especially when driving. Second-generation agents available in the United States (U.S.) (e.g., cetirizine, desloratadine, fexofenadine, levocetirizine, loratadine) has greatly reduced these CNS effects, making them the current treatments of choice in CIU, but their potency and tolerability profiles vary. Differences in duration of in vivo receptor occupancy may affect the potency of H1 antihistamines. Levocetirizine appears to have greater in vivo H1 receptor occupancy compared with later generation H1 antihistamines, which may confer an advantageous efficacy/safety profile. This has been confirmed in a recent head-to-head study showing that levocetirizine was more effective than desloratadine in improving pruritus in CIU patients. Fexofenadine has been shown to have a low occupancy of H1 antihistamine receptors in the brain, which reduces the likelihood of sedation. More studies are required to further assess receptor occupancy and other factors that may differentiate the second-generation H1 antihistamines.
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PMID:Second-generation antihistamines for the treatment of chronic idiopathic urticaria. 2048 Jul 93

The Center for Disease Control guidelines recommend desensitization to metronidazole in patients with trichomoniasis and hypersensitivity to metronidazole. There is only one published oral metronidazole desensitization protocol. The purpose of this study was to design a new, more gradual oral desensitization protocol to decrease systemic reactions that may occur when using the previously published protocol. We present two patients with presumed IgE-mediated allergy to metronidazole who underwent oral desensitization using our modified protocol. Case 1 was a 65-year-old woman with trichomoniasis who presented for metronidazole desensitization with a history of intraoperative anaphylaxis and positive skin tests to metronidazole. The patient tolerated six doses of the modified desensitization but developed systemic symptoms of nasal congestion and diffuse pruritus after the 25- and 100-mg doses. Both reactions were treated with intravenous (i.v.) antihistamines. Because of gastrointestinal irritation, the desensitization was completed at a dose of 250 mg orally every 6 hours. Case 2 was a 42-year-old woman with trichomoniasis and a history of hives immediately after administration of i.v. metronidazole who presented for desensitization. The patient had negative skin-prick and intradermal testing to metronidazole. She developed lip tingling and pruritus on her arms 15 minutes after the 10-mg dose. Fexofenadine at 180 mg was given orally and symptoms resolved. She tolerated the rest of the protocol without reaction and received a total dose of 2 g of metronidazole. Our oral metronidazole desensitization for presumed IgE-mediated reactions offers a second option for physicians wishing to use a more gradual escalation in dose.
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PMID:Modified oral metronidazole desensitization protocol. 2461 59