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

Arterial hypertension is a major risk factor for microangiopathic diabetic complications and associated with an increased cardiovascular morbidity and mortality. An intensified antihypertensive treatment reduces microangiopathic complications and cardiovascular morbidity and mortality in diabetic patients. Even in normotensive type 1 and type 2 diabetic patients, the treatment with ACE inhibitors may prevent the later development of diabetic nephropathy. Treatment with ACE inhibitors increases the concentrations of bradykinin, which is responsible for the side effects such as cough and urticaria in some patients. On the other hand, bradykinin may have beneficial intrarenal effects decreasing the intraglomerular pressure. The novel angiotensin II receptor type 1 antagonists do not influence the bradykinin concentrations and seem to be tolerated by patients suffering from chronic cough with ACE inhibitor therapy. It is still unclear whether the different intrarenal effects are of clinical relevance in the long-term treatment of diabetic patients. In studies with diabetic animals the nephroprotective effects of ACE inhibitors and angiotensin II type 1 receptor antagonists are comparable. It was shown that glucose and lipid metabolism is not influenced by treatment with angiotensin II type 1 receptor antagonists. Further compared to Felodipine the reduction of urinary albumin excretion rate (UAER) was more pronounced by Losartane in Chinese type 2 diabetic patients. Short-term studies directly comparing the renal effects of ACE inhibitors with AT II type 1 receptor antagonists revealed similar reduction of blood pressure and albumin excretion rate in patients with diabetic nephropathy, so a combination of both substances might be useful. Data from ongoing long-term trials are still missing. Further, it is unknown whether different phenotypes of the ACE gene (DD, II polymorphism) require different therapeutic options. In conclusion, treatment with angiotensin II receptor antagonists is well-tolerated and has no adverse effects on metabolic control in diabetic patients. The beneficial effect on microangiopathic complications however has to be proven in randomized long-term studies in direct comparison with ACE inhibitors, which were clearly shown to delay the development and progression of diabetic nephropathy.
 ...
PMID:[Angiotensin II type-1 receptor antagonists and diabetes mellitus]. 1145 Jan 65

Since adverse effects due to angiotensin-converting enzyme (ACE) inhibitors frequently occur in cutaneous locations, this review summarizes the spectrum of expected and unexpected adverse effects of these drugs, possible associated mechanisms, and their basic functions for dermatologists. ACE inhibitors block the activity of the metalloproteinase ACE by binding to its active site, thus displacing angiotensin I and preventing its conversion to vasopressive angiotensin II. Furthermore, ACE degrades bradykinin, substance P, enkephalins and some of the reproductive peptide hormones. The overall incidence of adverse effects to ACE inhibitors is estimated at 28%, approximately half of which occurs in the skin. General reactions are first-dose hypotension, hyperkalaemia and renal failure. Cutaneous reactions comprise life-threatening angioedema, pruritus, bullous eruptions, urticaria, other generalized rashes, photosensitivity and hair loss. ACE inhibitors thus mimic a broad variety of skin diseases, why these drugs should be thought of when sudden, unexplainable skin eruptions are observed.
 ...
PMID:Angiotensin-converting enzyme inhibitors as inducers of adverse cutaneous reactions. 1180 Jan 36

Urticaria is a classic cutaneous manifestation of drug allergy considered like the second most frequent drug eruption after maculopapular exanthemas. Most of the time drugs are responsible of acute urticaria lasting less than 24 hours. The mechanisms of these acute urticarial reactions are multiple, mostly related to an IgE-induced reaction. Nevertheless, some drugs can induce immune complexes and activate the complement cascade (sickness disease). Others may directly release mast cells mediators or activate complement by non immunologic mechanisms in the absence of antibody. In every case, these drugs are unable to generate urticaria during more than 6 weeks, time allowed for calling a chronic urticaria. However drugs like nonsteroidal anti-inflammatory drugs and acetysalicylic acid can, by a pharmacologic mechanism, exacerbate or trigger chronic urticaria. Angiotensin-converting enzyme inhibitors, by a defect of degradation of bradykinin, may also induced angioedemas. In this context, if an allergologic investigation is useful in the exploration of acute urticaria, it seems useless for chronic urticaria.
 ...
PMID:[Drug-induced chronic urticarias]. 1284 7

Drugs may cause urticaria by different mechanisms. The most well-known mechanism is the allergic reaction mediated by immunoglobulin (Ig)E antibodies, which induce acute generalized urticaria. Allergic reactions to beta-lactams are the most common cause of adverse drug reaction mediated by IgE antibodies. However, IgE antibodies are not always necessary to activate the release of mediators from mast cells and induce acute urticarias. Some drugs, such as opiates or codeine, act directly on mast cells, and others, such as aspirin and nonsteroidal anti-inflammatories, induce an exacerbation of chronic urticaria by a pharmacological mechanism involving the arachidonic acid metabolism. Additionally, angioedema is a wellknown complication of angiotensin-converting enzyme inhibitors by its action on bradykinin, which is a potent vasodilatator agent. Topical drugs, such as antibiotics, disinfectants, or anesthetics, may cause urticaria, which sometimes progresses to generalized urticaria and, more rarely, to anaphylactoid reactions.
 ...
PMID:Drug-induced urticarias. 1646 91

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.
 ...
PMID:[Angioedema]. 1800 29

Angioedema is a frequent disorder with multiple aetiologies. Angioedemas associated with urticaria are usually caused by histamine release and respond to anti-histamines and adrenalin. They include allergic angioedemas, anaphylactoid reactions (mostly drug-induced, e.g. NSAID), physical angioedemas and recurrent idiopathic angioedema. Bradykinin probably plays a causative role in the pathogenesis of ACE-inhibitor or angiotensin II receptor blocker related angioedemas, as well as in the pathogenesis of the rare hereditary or acquired C1-inhibitor deficiency angioedemas. Urticaria is then typically absent and anti-histamines, as well as adrenalin, are ineffective.
 ...
PMID:[The multiple etiologies of angioedema]. 1855 32

Urticaria and angioedema are common allergic manifestations and medications are one of common triggering factors. The most severe immediate drug reaction is anaphylaxis. Apart from the well established IgE-mediated immediate type hypersensitivity reactions, the pathogenesis of drug-induced urticaria, angioedema and anaphylaxis often remains obscure. In this article, emphasis is put on nonallergic reactions to the most commonly used drug groups of nonsteroidal antiinflammatory drugs, angiotensin-converting enzyme inhibitors, radiocontrast media, volume expanders and drugs used in general anesthesia. Urticaria is the second most common drug eruption after maculopapular exanthema. The mechanisms of acute urticarial reactions are multiple, mostly IgE mediated, but some drugs can induce immune complex reactions and activate complement cascade, while others can induce direct activation of mast cells and degranulation or activation of complement by non-immune mechanisms. With different types of medications different pathomechanisms are involved. Non-steroid anti-inflammatory drugs are thought to cause reaction due to cyclooxygenase-1 inhibition and overproduction of leukotrienes, blamed for cutaneous and respiratory symptoms. Angiotensin-converting enzyme inhibitors can cause fatal angioedema, which is partially explained with bradykinin excess and impairment of aminopeptidase P and dipeptidyl peptidase IV that are involved in the metabolism of substance P and bradykinin. It remains unknown what additional mechanisms are involved. Radiocontrast media and local anesthetics mostly cause nonallergic hypersensitivity reaction, but in rare cases true allergic reaction can occur. Dextran is known to cause IgG mediated, immune complex anaphylaxis and it is recommended to use human serum albumin as the safest colloid.
 ...
PMID:Nonallergic hypersensitivity to nonsteroidal antiinflammatory drugs, angiotensin-converting enzyme inhibitors, radiocontrast media, local anesthetics, volume substitutes and medications used in general anesthesia. 1938 16

Urticaria, a perplexing disease of ever-changing explanations, is being renovated almost everyday by newer facts and findings accumulated from different parts of the globe. Cost of the urticaria treatment gradually grows higher and higher whereas the ailment disturbs the quality of life very adversely. Disorder of coagulation cascade has recently thrown some new light into its mechanism. Non-allergic angioedema induced by bradykinin caused by genetic defects and ACE-inhibitors has also been noted. Role of H. pylori in the pathogenesis of urticaria has also been re-reviewed. Urticaria could sometimes mimic erythema multiforme and is termed urticaria multiforme. Skin biopsy showed features of vasculitis in good number of urticaria irrespective of clinical features. Contact sensitization showed positive results in certain cases thus proving contact urticaria. Topical clobetasol, systemic omalizumab and NB UVB have shown promising results in certain forms of urticaria.
 ...
PMID:What'S new in urticaria? 2016 64

Hereditary angioedema (HAE) is an inherited disorder characterized by recurrent, circumscribed, non-pitting, non-pruritic, and rather painful subepithelial swelling of sudden onset, which fades during the course of 48-72 hours, but can persist for up to 1 week. Lesions can be solitary or multiple, and primarily involve the extremities, larynx, face, esophagus, and bowel wall. Patients with HAE experience angioedema because of a defective control of the plasma kinin-forming cascade that is activated through contact with negatively charged endothelial macromolecules leading to binding and auto-activation of coagulation factor XII, activation of prekallikrein to kallikrein by factor XIIa, and cleavage of high-molecular-weight kininogen by kallikrein to release the highly potent vasodilator bradykinin. Three forms of HAE have currently been described. Type I and type II HAE are rare autosomal dominant diseases due to mutations in the C1-inhibitor gene (SERPING1). C1-inhibitor mutations that cause type I HAE occur throughout the gene and result in truncated or misfolded proteins with a deficiency in the levels of antigenic and functional C1-inhibitor. Mutations that cause type II HAE generally involve exon 8 at or adjacent to the active site, resulting in an antigenically intact but dysfunctional mutant protein. In contrast, type III HAE (also called estrogen-dependent HAE) is characterized by normal C1-inhibitor activity. The diagnosis of HAE is suggested by a positive family history, the absence of accompanying pruritus or urticaria, the presence of recurrent gastrointestinal attacks of colic, and episodes of laryngeal edema. Estrogens may exacerbate attacks, and in some patients attacks are precipitated by trauma, inflammation, or psychological stress. For type I and type II HAE, diminished C4 concentrations are highly suggestive for the diagnosis. Further laboratory diagnosis depends on demonstrating a deficiency of C1-inhibitor antigen (type I) in most kindreds, but some kindreds have an antigenically intact but dysfunctional protein (type II) and require a functional assay to establish the diagnosis. There are no particular laboratory findings in type III HAE. Prophylactic administration of either 17alpha-alkylated androgens or synthetic antifibrinolytic agents has proven useful in reducing the frequency or severity of attacks. Plasma-derived C1-inhibitor concentrate, recombinant C1-inhibitor, ecallantide (DX88; a plasma kallikrein inhibitor) and icatibant (a bradykinin B(2) receptor antagonist) have demonstrated significant efficacy in the treatment of acute attacks, whereas the C1-inhibitor concentrate has also provided a significant benefit as long-term prophylaxis. However, these drugs are not licensed in all countries and are not always readily available.
 ...
PMID:Hereditary angioedema in childhood: an approach to management. 2059 9

Inhalant abuse is the intentional inhalation of chemical vapors or volatile substance to achieve a euphoric effect. Although no statistical data are reported yet, inhalant abuse is potentially life-threatening and has resulted in a wide range of toxic effects such as central nervous system depression, seizures, aspiration, cardiac arrhythmia, asphyxiation, hypoxia, metabolic acidosis, and sudden death among others. We are reporting a 25-year-old white man who was brought to the emergency department after inhaling aerosolized computer-cleaning spray composed of difluoroethane. He was found to have marked upper and lower lip facial swelling consistent with angioedema. The patient also had a prolonged QT interval, mild inspiratory stridor, but no urticaria. In this case, we believe the difluoroethane-related angioedema represents either idiopathic or bradykinin-induced angioedema.
 ...
PMID:Inhalant abuse of computer cleaner manifested as angioedema. 2129 30


<< Previous 1 2 3 4 5 Next >>