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)

Angioedema without urticaria is a clinical syndrome characterised by self-limiting local swellings involving the deeper cutaneous and mucosa tissue layers. Most occurrences of angioedema respond to treatment with a histamine H1 receptor blocker (antihistamine) because they are an allergic or parallergic reaction. A small number of cases do not respond to antihistamine treatment. Such cases tend to occur in patients with deficiency or dysfunction of the inhibitor of the first component of the complement (C1-INH), but more rarely can occur in patients with other conditions and as an adverse drug reaction. Angioedema is well documented in patients taking ACE inhibitors. Considering that 35 to 40 million patients are treated worldwide with ACE inhibitors, this drug class could account for several hundred deaths per year from laryngeal oedema. ACE inhibitors certainly do not mediate angioedema through an allergic or idiosyncratic reaction. For this reason the relationship with this drug is often missed and consequently quite underestimated. Rare instances of angioedema have also been reported with angiotensin II receptor antagonists. This adverse effect seems to occur less frequently with angiotensin II receptor antagonists than with ACE inhibitors. However, we do not know whether this adverse effect has the same mechanism with the 2 classes of medications. Some cases of severe angioedema have been recently reported after treatment with fibrinolytic agents. Scattered reports suggest the possibility of angioedema associated with the use of estrogens, antihypertensive drugs other than ACE inhibitors, and psychotropic drugs. Angioedema can also occur with nonsteroidal anti-inflammatory drugs. Prevention of angioedema relies first on the patient history. Estrogen and ACE inhibitors should be avoided in a patient with congenital or acquired C1-INH deficiency. In the case of ACE inhibitors, the appearance of angioedema following long term treatment does not lessen the probability that such an agent could be the cause. The most important action to take in a patient with suspected drug-induced angioedema is to discontinue the pharmacological agent. Epinephrine (adrenaline), diphenydramine and intravenous methylprednisolone have been proposed for the medical management of airway obstruction, but so far no controlled studies have demonstrated their efficacy. If the acute airway obstruction leads to life-threatening respiratory compromise an emergency cricothyroidotomy must be performed.
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PMID:Drug-induced angioedema without urticaria. 1148 Apr 92

This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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PMID:Breathless. 1196 14

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

Oral contraceptives (OCs) can affect the skin through their hormonal effects or through iatrogenic effects associated with their toxicity in certain individuals. They may also be beneficial in certain androgen-dependent dermatoses. Toxic effects of OCs are rare but potentially serious; they should be diagnosed early and require permanent termination of OC use. The clinical manifestations are variable and not specific to the medication. The most frequently reported manifestations are allergic vascularities which may lead to serious renal complications, fixed pigmented erythema, urticaria, which may have other etiologic factors, and lichenoid eruptions. Combined OCs, because of their estrogen content, may cause sensitivity to light in susceptible women. Other dermatoses can be initiated or aggravated by OCs without direct relation to their hormonal effects. OCs are therefore contraindicated if there is a personal or family history of porphyries or a personal history of systemic lupus erythematosus, erythema nouex, herpes gestationis, or malignant melanoma. Hormonal-related dermatological effects caused by either progestins or estrogens have become less frequent as dose levels have declined. Chloasma, either melasma or a poorly defined spotty pigmentation, accounts for 2/3 of cases of OC-related dermatoses. It is more common in women of Mediterranean background. 80% of affected OC users have a history of "mask of pregnancy", but the condition is also found in nulliparas. Exposure to sunlight is a factor. Women with a history of chloasma of pregnancy and dark coloring should not use OCs. Seborrhea is directly related to the androgen effect of OCs and is less likely to occur with 17 OH progesterone derivatives than with 19 norsteroid derivatives. The role of androgens in acne is well known, but 2 other factors are necessary: an anomaly in keratinization and proliferation of corynebacterium acnes, a saprophyte of the follicles. OCs do not necessarily need to be suspended during well-conducted acne treatment. Alopecia is rare but difficult to diagnose because of its psychological aspects. Androgenic alopecia is aggravated by progestins derived from 19 norsteroids. True hirsutism caused by an androgen-producing ovarian pathology is not related to OC use. Estrogens are incriminated in the etiology of telangiectasies, permanent dilatations of the arterioles. Once developed the condition does not regress and requires treatment with sclerosing agents, electrocoagulation, or laser. The various dermatological risk factors should be ruled out before prescription of an OC. Classic contraceptive pills are not commonly used in treatment of common acne because the strongly estrogenic climate required for therapeutic utility carries the risk of hypertriglyceridemia, thrombophlebitis, and possibly carcinogenesis. The recent development of pills containing the antiandrogen cyproterone acetate instead of a progestin in combination with ethinyl estradiol reduces androgenic effects in women. This pill may be useful in cases of severe acne, severe seborrhea, androgenic alopecia, or excessive facial hair.
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PMID:[Cutaneous effects in hormonal contraception]. 1228 Dec 76

The incidence of cutaneous effects of oral contraceptives (OCs) is estimated at 2.7-5%. Secondary effects directly attributable to the hormonal action of OCs include melasma, acne and hyperseborrhea, alopecia, and cutaneous lesions of vascular origin. Melasma or chloasma accounts for about 2/3 of all cutaneous side effects of OCs. It appears from 1 month-3 years after the start of OC use, its frequency increasing with dose and duration of use. Pigmentation appears to accentuate the symptoms in brunettes rather than predisposing them to melasma. Exposure to the sun plays a certain role, but use of a low dose OC and effective sun protection are not enough to reverse the pigmentation. These melasmas regress more slowly than after pregnancy and many remain definitive. The influence of OCs on acne is variable, with some OCs provoking sebaceous hypersecretion and some improving acne enough to be used for treatment. For the therapeutic effect to be observed, the estrogen dose must be sufficient to offset the androgenic effect of the progestin. Combined pills containing the strong antiandrogen cyproterone acetate should control acne if other, less androgenic progestins fail. Alopecia is a very rare effect of OCs and its appearance may even reflect simple coincidence. Vascular complications of combined OCs are dependent on estrogens and may include such manifestations as telangiectasias, angiomas, and livedo reticularis. Some secondary cutaneous effects are probably not due to a hormonal influence. They are less well known than the direct hormonal effects, and publications concerning the often detail isolated observations that are difficult to interpret. Reactions of hypersensitivity or allergy to combined OCs may include urticaria and eczema. A history of OC use should be sought in all women presenting with erythema nodosum and the OCs should be discontinued. Pruritus and jaundice may be observed in 1 OC user in 100,000. They indicate a cholestatic hepatitis for which estrogens are responsible. Most patients developing the condition have already had pruritus or jaundice during pregnancy; such a history contraindicates OC use. Several dermatological and systemic disorders are aggravated by OC use. Hereditary angioedema, herpes gestationis, porphyries, and systemic lupus erythematosus are exacerbated by OC use. The role of OCs in malignant melanomas remains controversial.
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PMID:[Dermatological complications caused by oral contraceptives]. 1234 76

Although frequently reported as an aetiology for chronic angioneurotic oedema or urticaria, food allergy is often a diagnosis proposed in the absence of more convincing evidence, as illustrated by the disappointing results of eviction regimens. We report a series of women with an initial diagnosis of food allergy, but in whom the role of oral contraceptives was subsequently demonstrated. Detailed medical history was obtained from 26 young women presenting with chronic angioneurotic oedema or urticaria initially attributed to food allergy, but in whom C1-esterase inhibitor (C1 INH) deficiency was demonstrated. We investigated the effects of oral contraception on C1 INH levels, C1 INH activity and clinical symptoms of these patients. Discontinuation of oral contraception induced an increase in C1 INH levels and C1 INH activity, associated with recovery or marked improvement of the clinical symptoms formerly attributed to food allergy. The relatively high frequency of women taking cyproterone acetate in this population appeared to be a remarkable finding. Replacement of the initial contraception containing ethinylestradiol by a progestogen maintained or even accentuated these good therapeutic results. Exogenous oestrogens, such as those contained in most oral contraceptives, may play an iatrogenic role in the aetiology of chronic angioneurotic oedema or urticaria.
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PMID:Exogenous oestrogen as an alternative to food allergy in the aetiology of angioneurotic oedema. 1250 53

We analyzed the alarm pheromone components from five colonies of Africanized honeybees and three colonies of European honeybees collected in Mexico. Analyses revealed a novel alarm pheromone component that was only present in appreciable quantities in the Africanized bee samples. Analysis of the mass spectrum and subsequent synthesis confirmed that this compound is 3-methyl-2-buten-1-yl acetate (3M2BA), an unsaturated derivative of IPA. In Africanized honeybees, sampling from stings of guards showed that 3M2BA was present at levels of 0-38% the amount of isoamyl acetate (IPA). Behavioral assays from three colonies each of Africanized and European bees showed that 3M2BA recruited worker bees from hives of both Africanized bees and European bees at least as efficiently as isopentyl acetate IPA, a compound widely reported to have the highest activity for releasing alarm and stinging behavior in honeybees. However, a mixture of of 3M2BA and IPA (1:2) recruited bees more efficiently than either of the compounds alone. None of the compounds differed in their efficacy for inducing bees to pursue the observers.
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PMID:Discovery of 3-methyl-2-buten-1-yl acetate, a new alarm component in the sting apparatus of Africanized honeybees. 1273 69

Caffeic acid phenethyl ester (CAPE), which is derived from the propolis of honeybee hives, has been shown to reveal anti-inflammatory properties. Since T-cells play a key role in the onset of several inflammatory diseases, we have evaluated the immunosuppressive activity of CAPE in human T-cells, discovering that this phenolic compound is a potent inhibitor of early and late events in T-cell receptor-mediated T-cell activation. Moreover, we found that CAPE specifically inhibited both interleukin (IL)-2 gene transcription and IL-2 synthesis in stimulated T-cells. To further characterize the inhibitory mechanisms of CAPE at the transcriptional level, we examined the DNA binding and transcriptional activities of nuclear factor (NF)-kappaB, nuclear factor of activated cells (NFAT), and activator protein-1 (AP-1) transcription factors in Jurkat cells. We found that CAPE inhibited NF-kappaB-dependent transcriptional activity without affecting the degradation of the cytoplasmic NF-kappaB inhibitory protein, IkappaBalpha. However, both NF-kappaB binding to DNA and transcriptional activity of a Gal4-p65 hybrid protein were clearly prevented in CAPE-treated Jurkat cells. Moreover, CAPE inhibited both the DNA-binding and transcriptional activity of NFAT, a result that correlated with its ability to inhibit phorbol 12-myristate 13-acetate plus ionomycin-induced NFAT1 dephosphorylation. These findings provide new insights into the molecular mechanisms involved in the immunomodulatory and anti-inflammatory activities of this natural compound.
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PMID:Caffeic acid phenethyl ester inhibits T-cell activation by targeting both nuclear factor of activated T-cells and NF-kappaB transcription factors. 1461 83

Urticaria, angioedema, etc., and cross-reactions with ACE inhibitors.
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PMID:Cutaneous adverse effects of angiotensin-II receptor antagonists. 1732 83

Angioedema can be a symptom of anaphylaxis; it may be more hazardous that the circulatory collapse in otherwise healthy patients. Angioedema can be part of IgE- and histamine-mediated allergic reactions or part of NSAID-induced hypersensitivity with disturbances in arachidonic acid metabolism. If angioedema occurs without urticaria or other symptoms of anaphylaxis, it is usually mediated by increased bradykinin synthesis (HANE, EANE) or reduced metabolism (ACE inhibitors). These observations have led to new therapeutic approaches in HANE. Icatibant is a bradykinin-receptor-2 antagonist and blocks bradykinin-induced angioedema in HANE. How applicable this will be to ACE-inhibitor angioedema remains to be seen.
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PMID:[Angioedema]. 1800 29


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