Urticaria histamine

Allergic urticaria. Histamine and other pro-inflammatory substances are released from mast cells in the skin and tissues in response to the binding of allergen-bound IgE antibodies to high-affinity cell-surface receptors. Basophils and other inflammatory cells release histamine and other mediators, and are thought to play an important role, especially in chronic urticarial diseases. 

Cetirizine competitively antagonizes histamine at the Hi-receptor site and is indicated in the symptomatic relief of symptoms (e.g., nasal, nonnasal) associated with seasonal and perennial allergic rhinitis treatment of uncomplicated skin manifestations of chronic idiopathic urticaria. Histamine is a potent vasodilator, bronchial smooth-muscle constrictor, and stimnlant of nociceptive itch nerves. In addition to histamine, mnltiple chemical itch mediators can act as pruritogens on C-fibers, including neuropeptides, prostaglandins, serotonin, acetylcholine, and bradykinin. Furthermore, new receptor systems such as vanilloid, opioid, and canna-binoid receptors on cutaneous sensory nerve fibers that may modulate itch offer novel targets for antipruritic therapy. 

Hide M, Francis DM, Grattan CEH, Hakimi J, Kochan JP, Greaves MW Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med 1993 328 1599. Sd... 

Bruising, local irritation, mild pain, erythema, histamine-like reactions, and hematoma can occur at the site of injection. Hypersensitivity reactions involving chills, fever, urticaria, and rarely bronchospasm, nausea, vomiting, and shock have been reported in patients with HIT. Long-term UFH has been reported to cause alopecia, priapism, hyperkalemia, and osteoporosis. 

Histamine release Urticaria, pruritus, rarely exacerbation of asthma (varies among agents)... 

This second-generation histamine HI receptor blocker was put on the world market in the 1980s for the relief of symptoms associated with seasonal allergic rhinitis and chronic idiopathic urticaria [14], Janssen Pharmaceuticals marketed this dmg under the brand name Hismanal. The major benefit of these antihistamines was their... 

Kaplan AP, Horakova Z, Katz SI Assessment of tissue fluid histamine levels in patients with urticaria. J Allergy Clin Immunol 1978 61 350-354. 

Different people display individual patterns of susceptibility to biogenic amines in foods. Clinical signs of histamine poisoning are more severe in people taking medications which inhibit enzymes that normally detoxify histamine in the intestines. Symptoms may be gastrointestinal (nausea, vomiting, diarrhea), circulatory (hypotension), or cutaneous (rash, urticaria, palpitations, tingling. 

Drug-specific antibodies of the IgE type combine via their Fc moiety with receptors on the surface of mast cells. Binding of the drug provides the stimulus for the release of histamine and other mediators. In the most severe form, a life-threatening anaphylactic shock develops, accompanied by hypotension, bronchospasm (asthma attack), laryngeal edema, urticaria, stimulation of gut musculature, and spontaneous bowel movements (p. 326). 

Unwanted effects produced by d-tu-bocurarine result from a nonimmune-mediated release of histamine from mast cells, leading to bronchospasm, urticaria, and hypotension. More commonly, a fall in blood pressure can be attributed to ganglionic blockade by d-tu-bocurarine. 

Management of pruritus caused by allergic conditions such as chronic urticaria, atopic and contact dermatoses and in histamine-mediated pruritus. 

The indications for Hi-antihistaminics are derived from their mechanism of action all conditions in which a histamine release, mainly as sequel of an allergic reaction (bronchial asthma, hey fever, urticaria, allergic reactions to food or drugs), dominates the clinical symptoms. They can be used pro-phylactically or in acute situations, even by intravenous application. 

Mecfianism of Action An ethanolamine that competes with histamine on effector cells in the GI tract, blood vessels, and respiratory tract. Therapeutic Effect Relieves allergy symptoms, including urticaria, rhinitis, and pruritus. 

Mechanism of Action A nonsedating antihistamine that exhibits selective peripheral histamine Hi-receptor blocking action. Competes with histamine at receptor sites. Therapeutic Effect Prevents allergic responses mediated by histamine, such as rhinitis and urticaria. 

Mechanism of Action A phenothiazine that acts as an antihistamine, antiemetic, and CNS-antipsychotiC typical hypnotic. As an antihistamine, inhibits histamine at histamine receptor sites. As an antiemetic, diminishes vestibular stimulation, depresses labyrinthine function, and acts on the chemoreceptor trigger zone. As a sedative-hypnotic, produces CNS depression by decreasing stimulation to the brainstem reticular formation. Therapeutic Effect Prevents allergic responses mediated by histamine, such as rhinitis, urticaria, and pruritus. Prevents and relieves nausea and vomiting. Pharmacokinetics ... 

H5 ersensitivity reactions To prevent allergic reactions or to treat their symptoms, in which histamine is the primary mediator, the H -antagonists are the drugs of choice and are often quite effective. They are used primarily to treat allergic reactions produced by the release of histamine e.g., edematous states, pruritus, allergic rhinitis and urticaria. They are generally more effective in acute conditions and are used only for symptomatic relief. 

The newer antihistaminics agents e.g. Azelastme inhibits histamine release and also inflammatory reactions evoked by leukotrienes and plasma activating factor (PAF). It is used for seasonal and perennial allergic rhinitis in the form of nasal spray. Mizolastine, a non-sedating antihistaminic is used in allergic rhinitis and urticaria. Ebastine, another non-sedating antihistaminic is used in nasal and skin allergies. 

Numerous compounds capable of antagonising the effects of histamine are available. The main therapeutic role of these drugs is in the treatment of allergic diseases involving IgE-mediated hypersensitivity, such as allergic rhinitis, hay fever, and urticaria (Table 15.2). The main Table 15.2 Clinical uses of Hlantagonists... 

Histamine was synthesized in 1907 and later isolated from mammalian tissues. Early hypotheses concerning the possible physiologic roles of tissue histamine were based on similarities between the effects of intravenously administered histamine and the symptoms of anaphylactic shock and tissue injury. Marked species variation is observed, but in humans histamine is an important mediator of immediate allergic (such as urticaria) and inflammatory reactions, although it plays only a modest role in anaphylaxis. Histamine plays an important role in gastric acid secretion (see Chapter 62) and functions as a neurotransmitter and neuromodulator (see Chapters 6 and 21). Newer evidence indicates that histamine also plays a role in chemotaxis of white blood cells. 

Histamine is formed by decarboxylation of the amino acid l -histidine, a reaction catalyzed in mammalian tissues by the enzyme histidine decarboxylase. Once formed, histamine is either stored or rapidly inactivated. Very little histamine is excreted unchanged. The major metabolic pathways involve conversion to /V-methylhistamine, methylimidazoleacetic acid, and imidazoleacetic acid (IAA). Certain neoplasms (systemic mastocytosis, urticaria pigmentosa, gastric carcinoid, and occasionally myelogenous leukemia) are associated with increased numbers of mast cells or basophils and with increased excretion of histamine and its metabolites. 

Histamine-induced edema results from the action of the amine on Hi receptors in the vessels of the microcirculation, especially the postcapillary vessels. The effect is associated with the separation of the endothelial cells, which permits the transudation of fluid and molecules as large as small proteins into the perivascular tissue. This effect is responsible for urticaria (hives), which signals the release of histamine in the skin. Studies of endothelial cells suggest that actin and myosin within these cells contract, resulting in separation of the endothelial cells and increased permeability. 

Diphenhydramine Competitive antagonism at Hi receptors Reduces or prevents histamine effects on smooth muscle, immune cells also blocks muscarinic and adrenoceptors highly sedative IgE immediate allergies, especially hay fever, urticaria some use as a sedative, antiemetic, and antimotion sickness drug Oral and parenteral t duration 4-6 h Toxicity Sedation when used in hay fever, muscarinic blockade symptoms, orthostatic hypotension Interactions Additive sedation with other sedatives, including alcohol some inhibition of CYP2D6, may prolong action of some 13 blockers... 

Therapeutic doses of the opioid analgesics produce flushing and warming of the skin accompanied sometimes by sweating and itching CNS effects and peripheral histamine release may be responsible for these reactions. Opioid-induced pruritus and occasionally urticaria appear more frequently when opioid analgesics are administered parenterally. In addition, when opioids such as morphine are administered to the neuraxis by the spinal or epidural route, their usefulness may be limited by intense pruritus over the lips and torso. 

Insulin allergy, an immediate type hypersensitivity, is a rare condition in which local or systemic urticaria results from histamine release from tissue mast cells sensitized by anti-insulin IgE antibodies. In severe cases, anaphylaxis results. Because sensitivity is often to noninsulin protein contaminants, the human and analog insulins have markedly reduced the incidence of insulin allergy, especially local reactions. 

Stimulated platelets release arachidonic acid rapidly from their phospholipids, apparently as a result of activation of phospholipase A2. The released arachidonate can in turn be metabolized to endoperoxides and thromboxane A2 (Chapter 21). These compounds are also potent activators of platelets and cause a self-activating or autocrine effect.1) While PAF has a beneficial function, it can under some conditions contribute in a dangerous way to inflammation and to allergic responses including anaphylaxis,) asthmag and cold-induced urticaria.1 Although the effect of PAF is separate from those of histamine and of leukotrienes, these agents may act cooperatively to induce inflammation.1... 

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