Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: CAS:1668-19-5 (Doxepin)
104 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doxepin binds to intact astrocytes in primary cultures. The binding is competitively displaceable by excess cold doxepin and it is pronounced (Bmax = 27 nmol/mg protein) but the affinity is rather low (KD = 30 microM). The binding is inhibited by other antidepressants (amitriptyline, desipramine, tranylcypromine, iprindole) and propranolol but not by isoproterenol. Nevertheless, doxepin counteracts effectively the increase in the production of cyclic AMP evoked by isoproterenol.
PMID:Doxepin, a tricyclic antidepressant, binds to normal, intact astroglial cells in cultures and inhibits the isoproterenol-induced increase in cyclic AMP production. 626 30

Randomized double-blind trials using doxepin and several conventional antihistamines were carried out for treatment of patients with idiopathic cold urticaria. In the first double-blind trial, eight of nine patients preferred doxepin (10 mg three times daily) to cinnarizine (10 mg three times daily). In the second double-blind trial, the results of ice cube tests suppressing the effect of cyproheptadine (4 mg three times daily), doxepin (10 mg three times daily), and hydroxyzine (10 mg three times daily) did not statistically differ. However, doxepin was subjectively the most effective and it had fewer side effects than other treatments that were compared. Doxepin effectively suppressed the wheal and itching responses and shortened the duration of the wheal response in the ice cube test in all patients with cold urticaria who were studied.
PMID:Comparison of cinnarizine, cyproheptadine, doxepin, and hydroxyzine in treatment of idiopathic cold urticaria: usefulness of doxepin. 648 Sep 53

Previous studies show that oral antihistamines affect the weal and flare response to intradermal injections of the inflammatory mediators platelet-activating factor (PAF) and bradykinin (BK). The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on weal and flare responses to PAF and BK in healthy non-atopic human volunteers. The effects of doxepin on PAF responses were investigated, as there is evidence that doxepin may have direct anti-PAF effects in addition to its known antihistaminic actions. Terfenadine significantly reduced weal and flare responses to PAF (mean reduction 53 and 73%, respectively) and flare responses to BK (mean reduction 78%) but had no effect on weal responses to BK. Doxepin significantly reduced both weal and flare responses to PAF (mean reduction 43 and 68%, respectively, at higher doses of PAF). Cimetidine had no effect on weal or flare responses to PAF or BK. These findings suggest that the flare response to intradermal BK is mediated via histamine release while the weal response is not. The effects of the various antagonists of PAF-induced responses suggest that its effects too may be mediated via histamine, the similarity of the effects of terfenadine and doxepin on these responses indicating that the effects of doxepin may be due to its known antihistamine activity rather than to any specific PAF-antagonistic properties. Platelet-activating factor (PAF) is a phospholipid which is released from a wide range of cell types and also from vascular endothelium. PAF is formed by the conversion of ether-linked phospholipids initially to the biologically inactive lyso-PAF and then by acetylation to PAF. Intradermal injection of PAF in human skin causes vasodilatation and increased vascular permeability, producing a weal and flare response with accompanying pruritus. Bradykinin (BK) is a vasoactive polypeptide formed by the action of enzymes known as kallikreins on inactive precursors called kininogens. Its effects include an increase in blood flow and vascular permeability and stimulation of the release of prostaglandins and histamine. On intradermal injection in human skin it causes a weal and flare response with associated pain rather than pruritus. Previous studies have suggested that the weal and flare response to PAF may be mediated in part by histamine release. Given that BK is known to cause histamine release it appears possible that the responses to both compounds may be modified by conventional antihistamines. Experiments based on this premise have found that antihistamines have a pronounced effect on the flare response to PAF but a less marked effect on weal responses. The weal response to BK was unaffected by systemic antihistamines but studies have produced conflicting results with regard to effects on the flare response. The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on PAF- and BK-induced weal and flare responses in healthy, non-atopic human volunteers. Based on the treatment of cold urticaria it has been suggested that doxepin, which has known H1- and H2-antagonistic effects, may in addition show specific anti-PAF activity. We compared the effects of doxepin on PAF-induced intradermal responses with those of terfenadine and cimetidine in this study.
PMID:Effects of H1- and H2-antihistamines on platelet-activating factor and bradykinin-induced inflammatory responses in human skin. 868 66

Cold urticaria is characterized by the development of urticaria, usually superficial and/or angioedematous reaction after cold contact. It was found predominantly in young women. The diagnosis is based on the history and ice cube test. Patients with a negative ice cube test may have represented systemic cold urticaria (atypical acquired cold urticaria) induced by general body cooling. The pathogenesis is poorly understood. Cold urticaria can be classified into acquired and familial disorders, with an autosomal dominant inheritance. Idiopathic cold urticaria is most common type but the research of a cryopathy is necessary. Therapy is often difficult. It is essential that the patient be warned of the dangers of swimming in cold water because systemic hypotension can occur. H1 antihistamines can be used for treatment of cold urticaria but the clinical responses are highly variable. The combination with an H2 antagonists is more effective. Doxepin may be useful in the treatment. Leukotriene receptor antagonists may be a novel, promising drug entity. In patients who do not respond to previous treatments, induction of cold tolerance may be tried.
PMID:[Cold-induced urticaria]. 1238 50

The search for evidence based information and its evaluation for planning the care of a woman with pruritus without visible signs on her skin is exemplified and described in this article. Literature was sought with the key words "itch", "pruritus", and "elderly" in medline, Cinahl and the Cochrane library. Retrieved studies were appraised by the criteria for valid information of evidence based nursing. Most pruritus studies were about pruritus with skin rash or about pruritus connected to liver or renal failure. Randomised controlled trials about the treatment of pruritus were characterised by small sample sizes or were done with only men or women. The little knowledge found in these studies did not help resolve the complex individual situation of the patient. Treatment suggestions from the studies: to assess the causes and exacerbating factors of pruritus; to wash the skin with water only, e.g. without soap; to emulsify the skin with Vaseline or oil at least once daily; to prevent too much heat by covering the patient just enough for him or her to feel no cold; prescribing Atarax, a histamin inhibitor of the first generation at night time; to try the antidepressant drug Doxepin; and emulsification with alcohol, menthol and cool water. There is no evidence to predict results of any one of these suggested interventions. Further research regarding the pathophysiology and the effectiveness of interventions against pruritus is needed.
PMID:[Pruritus without skin manifestation--what kind of state of the art nursing intervention?]. 1461 17