Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among all the known drug intolerances, adverse reactions to heparin are not very common. No desensitization in patients with heparin hypersensitivity has ever been attempted. We report the case of a 55-year-old female patient with mitral stenosis and insufficiency, and tricuspid and aortic insufficiency. The patient underwent heparin treatment, and urticaria occurred with either s.c. calcium heparin or i.v. sodium heparin. Allergy testing (skin tests and patch tests) was negative. A pseudoallergic intolerance was diagnosed. Mitral valve replacement with the extracorporeal circulation method was necessary; therefore, heparin treatment was administered. A heparin rush desensitization together with antihistamine drugs (4 mg clorpheniramine maleate for 3 d) was started: 50 UI (0.5 mg) s.c. sodium heparin were first administered; within 4 d, 5000 UI (50 mg) sodium heparin was administered i.v. with no side-effects. A full-dosage heparin treatment was then administered and heart surgery was easily performed. During the postsurgical course, i.v. sodium heparin was smoothly replaced with s.c. calcium heparin (25,000 UI s.c. per day) and with oral anticoagulants (sodium warfarin).
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PMID:Rush desensitization in heparin hypersensitivity: a case report. 803 62

Treatment of chronic urticaria presents a challenge to both practitioner and patient. Traditional H1 antagonists with good efficacy but substantial side effects are being supplanted in many cases by nonsedating H1. Combinations of H1 and H2 antagonists offer improved results for selected patients. Second-line therapies include a wide range of drugs such as doxepin, dapsone, attenuated androgens, calcium antagonists, antimalarials, gold and methotrexate. The most effective and regularly used second-line agents are corticosteroids. These are best limited to short term crisis management, except in severe recalcitrant cases, and in patients with pressure urticaria or urticarial vasculitis. Further development and investigation of mast cell stabilisers and inhibitors of urticaria mediators other than histamine hold promise. A better understanding of the underlying pathogenesis remains the greatest hope of formulating rational and effective therapy.
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PMID:Pharmacologic therapy for urticaria. 911 75

Propolis is a resinous wax-like material that is used by bees as a glue-like matrix in their hives. The in vitro effect of propolis solutions was investigated on the microhardness of human dental enamel. The calcium concentration of the solution was 7.8 ppm, the pH values varied between 5 and 6. The fluoride concentration was negligible. The Vickers hardness number of exposed enamel showed a steady increase with the percentage of propolis in the solution. The microhardness increase may be attributed to particular components of mineralization activity in propolis.
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PMID:The effect of propolis exposure on microhardness of human enamel in vitro. 1062 Jan 58

Haptoglobin (Hp) is an acute phase reactant produced by hepatocytes. There is evidence for an immunomodulatory potential of Hp, though there is no clear evidence yet about the mechanisms of this action. We have previously shown that Hp interacts with the beta2-integrin CD11b/CD18. In addition, other investigators reported the binding of Hp to B lymphocytes through the CD22 receptor, and to neutrophils through two different receptors. In the present study, we investigated the interaction of haptoglobin with the human mast cell line HMC-1. We report that fluorescein isothiocyanate (FITC)-labelled haptoglobin binds to this cell line and that binding is increased by calcium in a dose- and time-dependent manner. Hp binding sites on HMC-1 were upregulated upon stimulation with phorbol myristate acetate (PMA)/A23187 and after treatment with anti-CD43 and anti-CD44 monoclonal antibodies (MoAbs). HMC-1 cells do not express either CD11b/CD18 or CD22 receptors, indicating that the haptoglobin-binding receptor on this cell line is different from the known receptors. Assessment of cell function showed that Hp inhibits the spontaneous growth of HMC-1 up till 40% at higher Hp concentrations, but it did not exhibit any effect on the expression of CD54 on the release of either tryptase or IL-1ra. In conclusion, haptoglobin binds specifically to human mast cells via a receptor different from CD11b/CD18 and CD22, and may play a role in the modulation of mast cell functions. Exploration of Hp effects in mast cell-dependent diseases such as allergic rhinitis and urticaria seems warranted.
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PMID:Haptoglobin interacts with the human mast cell line HMC-1 and inhibits its spontaneous proliferation. 1196 16

It is generally accepted that topical steroid ointment and anti-histamine drug are the first choice of the treatment on pruritic skin diseases such as contact dermatitis, urticaria, prurigo, or pruritus cutanea. Among these diseases, prurigo is one of the most refractory skin disease to the common therapies. In this review, we would like to summarize the effect of vitamin D(3) to refractory skin disease on the basis of our clinical study.
Clin Calcium 2004 Oct
PMID:[New perspective of vitamin D3 ointment--pruritic skin diseases: focused on prurigo]. 1557 46

Plasma exchange (PE) is a technique of extracorporeal blood purification which removes large molecular weight substances from plasma. The Department of Dialysis, Zagreb University Hospital Center's database, which includes data on 509 patients, or 4857 PE treatments, was retrospectively analyzed to test the safety of PE. A total of 231 adverse reactions were recorded (4.75% of treatments). The most common complications were paresthesias (2.7%), hematoma at the puncture site (2.4%), clotting (1.7%), mild to moderate allergic reactions (urticaria; 1.6%) and bleeding (0.06%). True anaphylactoid reactions were recorded in five procedures. The incidence of severe, potentially life-threatening adverse reactions was 0.12%. The prophylactic use of calcium and potassium was responsible for a low incidence of electrolyte disturbances. There was no lethal outcome associated with PE. When carried out by experienced staff, PE is a relatively safe procedure. The use of fresh frozen plasma is associated with a higher rate of adverse reactions.
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PMID:Complications of therapeutic plasma exchange: experience with 4857 treatments. 1620 13

Cysteinyl-leukotrienes (cysteinyl-LTs) exert a range of proinflammatory effects, such as constriction of airways and vascular smooth muscle, increase of endothelial cell permeability leading to plasma exudation and edema, and enhanced mucus secretion. They have proved to be important mediators in asthma, allergic rhinitis, and other inflammatory conditions, including cardiovascular diseases, cancer, atopic dermatitis, and urticaria. The classification into subtypes of the cysteinyl-LT receptors (CysLTRs) was based initially on binding and functional data, obtained using the natural agonists and a wide range of antagonists. CysLTRs have proved remarkably resistant to cloning. However, in 1999 and 2000, the CysLT1R and CysLT2R were successfully cloned and both shown to be members of the G-protein coupled receptors (GPCRs) superfamily. Molecular cloning has confirmed most of the previous pharmacological characterization and identified distinct expression patterns only partially overlapping. Recombinant CysLTRs couple to the Gq/11 pathway that modulates inositol phospholipids hydrolysis and calcium mobilization, whereas in native systems, they often activate a pertussis toxin-insensitive Gi/o-protein, or are coupled promiscuously to both G-proteins. Interestingly, recent data provide evidence for the existence of an additional receptor subtype that seems to respond to both cysteinyl-LTs and uracil nucleosides, and of an intracellular pool of CysLTRs that may have roles different from those of plasma membrane receptors. Finally, a cross-talk between the cysteinyl-LT and the purine systems is being delineated. This review will summarize recent data derived from studies on the molecular and cellular pharmacology of CysLTRs.
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PMID:Cysteinyl-leukotriene receptors and cellular signals. 1776 56

Jellyfish bites in Hungary are rare. Yet, from a differential diagnostic point of view this epizoonozis might gain importance given the ever-growing popularity of seaside tourism. A 10 year old female patient was stung by a jellyfish while sea-bathing in the Adriatic in the summer of 2005. A couple of minutes after the bite urticaria were formed in the contacted area accompanied by a burning and sore sensation. In a few hours the above lesions turned livid and the patient developed low-grade fever and general discomfort. In acute therapy she received thorough rinse with vinegar, antibiotic ointment and systemic calcium. General symptoms regressed within 24 hours and dermatological symptoms improved progressively. Finally, the patient grew symptomless in 4 weeks altogether due to general antihistamine and local antibiotic therapy. 3 months later the patient presented again with hyperaemic papules and an increasing itching and burning sensation in the previously jellyfish-contacted area. Histopathology showed vascular involvement and eosinophilic infiltration. The inflammatory symptoms gradually diminished to locally applied steroids in an occlusive bandage leaving behind hypopigmentation. Although bare-skin contact with the different poisonous jellyfish species usually do lead to the forming of dermatological symptoms, vascular involvement developed months after the encounter in the exposure site has seldom been published. The article covers the main potential symptoms of jellyfish stings--both local and general--going into details about the possible dermatological differential diagnoses. Furthermore, the most venomous jellyfish species, their geographical habitats, do's and don't-s of first aid, therapy and prevention are being briefly discussed by the authors.
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PMID:[Jellyfish sting. A case report]. 1808 81

Cysteinyl leukotrienes (LTC4, LTD4, LTE4) have a proinflamation effect, such as contraction of blood vessels smooth muscle and the respiratory tract, chemotaxis of proinflammatory cells increased endothelium cells permeability and mucus secretion. They are lipid mediators playing an important part in the pathophysiology of bronchial asthma, allergic rhinitis, atopic dermatitis, urticaria, cardiovascular system disorders and tumors. They act through at least four receptors from the rhodopsin gene family, lying in the area of GPCR genes superfamily--CYSLTR1, CYSLTR2, GPR17 and receptor for LTE4 (CYSLT(E)R). Their location, apart from small exceptions, is differentiated and typical for tissues. The highest CYSLTR1 expression was stated in the spleen, peripheral blood leucocytes, interstitial lung macrophage and smooth muscle cells. CYSLTR2 shows highest expression in the hearth, adrenal glands, placenta, spleen and peripheral blood leucocytes, and somewhat smaller in the brain. Biochemical and pharmacological study and the analysis of sequences have shown that all three types of receptors belong to the group of 7-transmembrane receptors--GPCR. The CYSLTR1 excitation power is distributed: LTD4>LTC4>LTF4, and CYSLTR2 LTC4=LTD4>LTE4. Cysteinyl leukotrienes receptors are coupled with the G(q/11) proteins and signal path leading to phosphatidylinositol hydrolysis (PI) and mobilization of intracellular calcium. These receptors are in vivo coupled with the PTX-sensitive G(q/11) protein or both G proteins. CYSLTR1 increases the metabolism of PI and intracellular calcium, activates MAPK kinases, induces differentiation and proliferation of cells, chemotaxis, actin reorganization, release of inflammation mediators and regulation of hematopoietic stem cells. CYSLTR2 also increases the concentration of intracellular calcium, stimulates the release of IL-8 and increases expression of early genes. It is connected to thrombosis, vessel damage, inflammation process and cell death. The existence of new, nuclear, localization of CYSLTR and coexistence with other membrane receptors is postulated. It is probable that they can crate homo- or heterodimers. This indicates the existence of new, previously not know actions of, cysteinyl leukotrienes and their receptors.
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PMID:[Cysteinyl leukotrienes and their receptors]. 2020 53

Exposure to low temperatures often causes allergic responses or urticaria. Similarly, menthol, a common food additive is also known to cause urticaria, asthma, and rhinitis. However, despite the obvious clinical implications, the molecular mechanisms responsible for inducing allergic responses to low temperatures and menthol have not been determined. Because a non-selective cation channel, transient receptor potential subtype M8 (TRPM8) is activated by cold and menthol, we hypothesized that this channel mediates cold- and menthol-induced histamine release in mast cells. Here, we report that TRPM8 is expressed in the basophilic leukemia mast cell line, RBL-2H3, and that exposure to menthol or low temperatures induced Ca(2+) influx in RBL-2H3 cells, which was reversed by a TRPM8 blocker. Furthermore, menthol, a TRPM8 agonist, induced the dose-dependent release of histamine from RBL-2H3 cells. When TRPM8 transcripts were reduced by siRNA (small interfering RNA), menthol- and cold-induced Ca(2+) influx and histamine release were significantly reduced. In addition, subcutaneous injection of menthol evoked scratching, a typical histamine-induced response which was reversed by a TRPM8 blocker. Thus, our findings indicate that TRPM8 mediates the menthol- and cold-induced allergic responses of mast cells, and suggest that TRPM8 antagonists be viewed as potential treatments for cold- and menthol-induced allergies.
Cell Calcium 2010 Oct
PMID:TRPM8 mediates cold and menthol allergies associated with mast cell activation. 2093 18


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