piperidines has been researched along with Dermatitis* in 14 studies
1 trial(s) available for piperidines and Dermatitis
Article | Year |
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Evaluation of slow-releasing diphenylpyraline in chronic urticaria and various kinds of dermatites.
Topics: Adolescent; Adult; Child; Child, Preschool; Chronic Disease; Delayed-Action Preparations; Dermatitis; Female; Follow-Up Studies; Histamine H1 Antagonists; Humans; Male; Middle Aged; Piperidines; Placebos; Pruritus; Tablets; Time Factors; Urticaria | 1971 |
13 other study(ies) available for piperidines and Dermatitis
Article | Year |
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Topical Janus kinase-signal transducers and activators of transcription inhibitor tofacitinib is effective in reducing nonatopic dermatitis chronic itch: A case series.
Topics: Dermatitis; Humans; Janus Kinases; Piperidines; Pruritus; Pyrimidines; Pyrroles | 2022 |
[Granulomatous rosacea-like dermatitis under therapy with tofacitinib].
The case of a 32-year-old female with ulcerative colitis who developed severe papulopustular dermatitis while undergoing treatment with the Janus kinase (JAK) inhibitor tofacitinib. Despite intensive topical therapy, treatment with oral corticosteroids and oral doxycycline was unable to achieve sufficient improvement. Hence, tofacitinib treatment needed to be discontinued. It is well known that the class of JAK inhibitors can cause infectious and allergic cutaneous side effects. However, sterile papulopustular dermatitis as a side-effect has rarely been reported to date.. Wir berichten von einer 32-jährigen Patientin mit Colitis ulcerosa, die unter Therapie mit dem JAK(Januskinase)-Inhibitor Tofacitinib eine massive papulopustulöse Dermatitis entwickelt hat. Trotz intensiver lokaltherapeutischer Maßnahmen und der Einnahme von Kortikosteroiden und Doxycyclin trat keine ausreichende Besserung ein, sodass die Tofacitinib-Behandlung beendet werden musste. Bekanntermaßen kann die Klasse der JAK-Inhibitoren zu infektiösen und allergischen Hautnebenwirkungen führen. Fälle von steriler papulopustulöse Dermatitis unter Therapie mit JAK-Inhibitoren sind allerdings bislang kaum berichtet worden. Topics: Adult; Dermatitis; Female; Humans; Piperidines; Pyrimidines; Pyrroles; Rosacea | 2021 |
Fever and Rash in an Adult: Varicella Re-infection in Conjunction with Newly Diagnosed Chronic Lymphocytic Leukemia.
Topics: Acyclovir; Adenine; Adult; Antiviral Agents; Chickenpox; Dermatitis; Fever; Humans; Leukemia, Lymphocytic, Chronic, B-Cell; Male; Piperidines; Pyrazoles; Pyrimidines | 2019 |
Intense Local Reaction at the Sites of Injection of Lipolytic Mesotherapy.
Topics: Abdomen; Amoxicillin-Potassium Clavulanate Combination; Anti-Inflammatory Agents; Benzimidazoles; Carnitine; Clobetasol; Dermatitis; Edema; Erythema; Female; Humans; Injections, Subcutaneous; Keratosis; Lipolysis; Mesotherapy; Middle Aged; Peptides; Phosphatidylcholines; Piperidines; Prednisone; Subcutaneous Fat; Thigh | 2017 |
Reversal of CD8 T-cell-mediated mucocutaneous graft-versus-host-like disease by the JAK inhibitor tofacitinib.
The utility of allogeneic hematopoietic stem cell transplantation is limited by graft-versus-host disease (GVHD), a significant cause of morbidity and mortality. Patients with GVHD exhibit cutaneous manifestations with histological features of interface dermatitis followed by scleroderma-like changes. JAK inhibitors represent a class of immunomodulatory drugs that inhibit signaling by multiple cytokines. Herein we report the effects of tofacitinib in a murine model of GVHD. Oral administration of tofacitinib prevented GVHD-like disease manifested by weight loss and mucocutaneous lesions. More importantly, tofacitinib was also effective in reversing established disease. Tofacitinib diminished the expansion and activation of murine CD8 T cells in this model, and had similar effects on IL-2-stimulated human CD8 T cells. Tofacitinib also inhibited the expression of IFN-γ-inducible chemoattractants by keratinocytes, and IFN-γ-inducible cell death of keratinocytes. Tofacitinib may be an effective drug for treatment against CD8 T-cell-mediated mucocutaneous diseases in patients with GVHD. Topics: Administration, Oral; Animals; Bone Marrow; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Cell Proliferation; Chemokines; Cytokines; Dermatitis; Gene Expression Regulation; Graft vs Host Disease; Hematopoietic Stem Cell Transplantation; Humans; Interleukin-2; Keratinocytes; Mice; Mice, Inbred C57BL; Piperidines; Protein Kinase Inhibitors; Pyrimidines; Pyrroles | 2014 |
Potent and orally bioavailable CCR4 antagonists: Synthesis and structure-activity relationship study of 2-aminoquinazolines.
Starting with a series of CC chemokine receptor-4 (CCR4) antagonists developed in a previous study, the potency was improved by replacing the pyrrolidine moiety of N-(4-chlorophenyl)-6,7-dimethoxy-2-(4-pyrrolidin-1-ylpiperidin-1-yl)quinazolin-4-amine 2 with a 3-(hydroxymethyl)piperidine. The resulting compound (1'-{4-[(4-chlorophenyl)amino]-6,7-dimethoxyquinazolin-2-yl}-1,4'-bipiperidin-3-yl)methanol 8ic was a strong inhibitor of human/mouse chemotaxis. Oral administration of 8ic showed anti-inflammatory activity in a murine model of acute dermatitis (oxazolone-induced contact hypersensitivity test) in a dose-dependent manner. Topics: Administration, Oral; Amines; Animals; Anti-Inflammatory Agents; Chemotaxis; Dermatitis; Disease Models, Animal; Humans; Mice; Piperidines; Quinazolines; Receptors, CCR4; Structure-Activity Relationship | 2009 |
Cream formulations protecting against cercarial dermatitis by Trichobilharzia.
Dermatitis caused by penetrating bird schistosome cercariae is an emerging global public health problem. Infections may be prevented by the use of topical formulations that inhibit cercarial skin penetration. We evaluated nine water resistant formulations by exposing treated arms of volunteers to Trichobilharzia szidati cercariae. Six formulations protected from cercarial invasion. However, after immersion of the treated skin in water (2 x 20 min), only two formulations offered full protection: (1) Safe Sea, a cream protecting against jelly fish, (2) niclosamide in water resistant sun protecting cream formulations at concentrations as low as 0.05%. In an in vitro system Safe Sea and a 0.1% niclosamide formulation caused a high damage rate in T. szidati (92% and 99% after 5 min; only niclosamide with lethal effect) but not in Schistosoma mansoni (1% and 72%; both formulations with lethal effect). However, a 1% niclosamide formulation damaged S. mansoni sufficiently (100% after 5 min) and might offer full penetration protection. Topics: Adult; Animals; Anthelmintics; DEET; Dermatitis; Dimethylpolysiloxanes; Dosage Forms; Humans; Lauric Acids; Middle Aged; Niclosamide; Piperidines; Propionates; Schistosomatidae; Time Factors; Trematode Infections | 2007 |
In vivo pharmacological characterisation of bilastine, a potent and selective histamine H1 receptor antagonist.
We set out to establish the in vivo histamine H(1) receptor antagonistic (antihistaminic) and antiallergic properties of bilastine.. In vivo antihistaminic activity experiments consisted of measurement of: inhibition of increase in capillary permeability and reduction in microvascular extravasation and bronchospasm in rats and guinea pigs induced by histamine and other inflammatory mediators; and protection against lethality induced by histamine and other inflammatory mediators in rats. In vivo antiallergic activity experiments consisted of measurement of passive and active cutaneous anaphylactic reactions as well as type III and type IV allergic reactions in sensitised rodents.. In the in vivo antihistaminic activity experiments, bilastine was shown to have a positive effect, similar to that of cetirizine and more potent than that of fexofenadine. The results of the in vivo antiallergic activity experiments showed that the properties of bilastine in this setting are similar to those observed for cetirizine and superior to fexofenadine in the model of passive cutaneous anaphylactic reaction. When active cutaneous anaphylactic reaction experiments were conducted, bilastine showed significant activity, less potent than that observed with cetirizine but superior to that of fexofenadine. Evaluation of the type III allergic reaction showed that of the antihistamines only bilastine was able to inhibit oedema in sensitised mice, although its effect in this respect was much less potent than that observed with dexamethasone. In terms of the type IV allergic reaction, neither bilastine, cetirizine nor fexofenadine significantly modified the effect caused by oxazolone.. The results of our in vivo preclinical studies corroborate those obtained from previously conducted in vitro experiments of bilastine, and provide evidence that bilastine possesses antihistaminic as well as antiallergic properties, with similar potency to cetirizine and superior potency to fexofenadine. Topics: Animals; Benzimidazoles; Bradykinin; Bronchial Spasm; Capillary Permeability; Cetirizine; Dermatitis; Dose-Response Relationship, Drug; Guinea Pigs; Histamine; Histamine Antagonists; Hypersensitivity; Male; Mice; Molecular Structure; Oxazolone; Piperidines; Rats; Rats, Wistar; Receptors, Histamine H1; Serotonin; Structure-Activity Relationship; Terfenadine; Time Factors | 2006 |
Norpiperidine imidazoazepines as a new class of potent, selective, and nonsedative H1 antihistamines.
Clinical doses of available H(1) antihistamines are limited mainly by sedative side effects. However, higher doses are often required to obtain optimal therapeutic activity, especially in dermatology. We report the synthesis of three norpiperidine imidazoazepines representative of a new class of selective and nonsedating H(1) antihistamines. The compounds were at least as potent as cetirizine and loratadine as measured by H(1) receptor binding affinity, by protection against compound 48/80- and histamine-induced lethality in rats and guinea pigs, respectively, and by skin reaction tests in rats, guinea pigs, and dogs. The compounds, in particular 3a, were less prone than the reference compounds to penetrate the brain and to occupy central H(1) receptors, suggesting absence of sedative side effects. In vitro and in vivo cardiovascular safety tests showed that 3a had no intrinsic potential to prolong ventricular repolarization or induce cardiac arrhythmias. Compound 3a has been selected for further clinical development, mainly for application in dermatology. Topics: Anaphylaxis; Animals; Arrhythmias, Cardiac; Benzazepines; Blood-Brain Barrier; CHO Cells; Cricetinae; Cricetulus; Dermatitis; Dermatologic Agents; Dogs; Drug Stability; Female; Guinea Pigs; Histamine H1 Antagonists, Non-Sedating; Hydrogen-Ion Concentration; Imidazoles; In Vitro Techniques; Male; Passive Cutaneous Anaphylaxis; Piperidines; Radioligand Assay; Rats; Rats, Wistar; Solubility; Spiro Compounds; Structure-Activity Relationship; Ventricular Function | 2005 |
Interactive contribution of NK(1) and kinin receptors to the acute inflammatory oedema observed in response to noxious heat stimulation: studies in NK(1) receptor knockout mice.
1. Scald injury in Sv129+C57BL/6 mice induced a temperature and time dependent oedema formation as calculated by the extravascular accumulation of [(125)I]-albumin. Oedema formation was suppressed in NK(1) knockout mice compared to wildtypes at 10 (P<0.01) and 30 min (P<0.001). However, at 60 min a similar degree of extravasation was observed in the two groups. 2. Kinin B(1) (des-Arg(10) Hoe 140; 1 micromol kg(-1)) and B(2) (Hoe 140; 100 nmol kg(-1)) antagonists caused an inhibition of oedema in wildtype mice at 10 and 30 min (P<0.001), but not at 60 min or at 30 min in NK(1) receptor knockout mice. 3. The inhibition of thermic oedema by des-Arg(10) Hoe 140 was reversed by des-Arg(9) bradykinin (0.1 micromol kg(-1); P<0.01) and also observed with a second B(1) receptor antagonist (des-Arg(9) Leu(8) bradykinin; 3 micromol kg(-1); P<0.01). Furthermore des-Arg(10) Hoe 140 had no effect on capsaicin (200 microg ear(-1)) ear oedema, but this was significantly reduced with Hoe 140 (P<0.05). 4. Scalding induced a large neutrophil accumulation at 4 h, as assessed by myeloperoxidase assay (P<0.001). This was not suppressed by NK(1) receptor deletion or kinin antagonists. 5. These results confirm an essential role for the NK(1) receptor in mediating the early, but not the delayed phase of oedema formation or neutrophil accumulation in response to scalding. The results also demonstrate a pivotal link between the kinins and sensory nerves in the microvascular response to burn injury, and for the first time show a rapid involvement of the B(1) receptor in murine skin. Topics: Administration, Topical; Animals; Bradykinin; Bradykinin Receptor Antagonists; Burns; Capsaicin; Cell Movement; Dermatitis; Edema; Hot Temperature; Injections, Intravenous; Mice; Mice, Inbred C57BL; Mice, Knockout; Neutrophils; Piperidines; Quinuclidines; Receptor, Bradykinin B1; Receptor, Bradykinin B2; Receptors, Bradykinin; Receptors, Neurokinin-1; Tachykinins; Time Factors | 2001 |
Allergic reactions to topical (surface) anesthetics with reference to the safety of tronothane (pramoxine hydrochloride).
Topics: Administration, Topical; Anesthetics; Anti-Inflammatory Agents; Benzocaine; Dermatitis; Dermatitis, Contact; Humans; Hydrocortisone; Hydroxybenzoates; Lidocaine; Morpholines; Ointments; Piperidines; Safety | 1980 |
[Local and general treatment of acute wet dermatitis and frostbites with 1-methyl-4-amino-N'-phenyl-N'-(2'-thenyl)-piperidine].
Topics: Anti-Allergic Agents; Dermatitis; Frostbite; Histamine H1 Antagonists; Humans; Piperidines | 1961 |
[Adaline toxicoderma with clinical aspect of Gougerot-Blum's pigmented purpuric lichenoid dermatitis].
Topics: Bridged-Ring Compounds; Dermatitis; Humans; Pharmaceutical Preparations; Piperidines; Purpura; Skin Diseases; Urea | 1950 |