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)

To identify and measure the incidence of adverse effects of the angiotensin converting enzyme inhibitor enalapril 13,713 patients were studied for one year by prescription-event monitoring. Precise information about the duration of treatment was available for 12,543 patients. The frequency of many events was calculated, including dizziness (483 patients; 3.9%), persistent dry cough (360; 2.9%), headache (310; 2.5%) hypotension (218; 1.7%), and syncope (155; 1.2%). Less common reactions included angioedema, urticaria, and muscle cramps. Altogether 1098 (8%) patients died and the notes of 913 of them (83%) were obtained for detailed scrutiny. With the exception of a few patients with renal failure who deteriorated during treatment (reported on separately), no death was attributed to enalapril. Enalapril was considered to be effective, even in patients with advanced cardiac failure. These results for enalapril are reassuring and provide further evidence of the value of prescription-event monitoring.
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PMID:Postmarketing surveillance of enalapril. I: Results of prescription-event monitoring. 284 1

Captopril was used for treatment resistant arterial hypertension in 17 dialysis patients. Excellent blood-pressure control with diastolic blood-pressure less than 95 mmHg was obtained in 10 out of 17 patients (59%), with captopril as only drug in 8 patients. Six patients have been treated more than 6 months and 4 patients have been on the treatment for 1 year. The dosage of captopril could be kept low with maintained antihypertensive and angiotensin converting enzyme blocking effects. The acute blood-pressure lowering effect of captopril in dialysis patients was correlated to the initial plasma renin activity (p less than 0.001) but not long-term treatment, which was successful also in several low-renin patients. A few adverse reactions were encountered, e.g. urticaria and bullous exanthema, but all resolved when captopril treatment was stopped. Plasma potassium increased only from 4.8 +/- 0.1 to 5.0 +/- 0.1 mmol/l at the end of 1 month's treatment. Captopril appears to be a valuable drug for treatment of arterial hypertension in dialysis patients and offers an alternative to bilateral nephrectomy for the management of treatment resistant hypertension in these patients.
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PMID:Captopril treatment in hypertensive dialysis patients. 676 61

Angioedema/urticaria secondary to ACE inhibitor drugs is an important clinical entity, which dermatologists should be aware of as they are so widely used and their use will undoubtedly increase. In addition to the obvious importance to the patient of promptly recognizing ACE inhibitor angioedema, uncovering the etiology of angioedema/urticaria is a rare and satisfying experience that can "make your day."
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PMID:The Fine Page: angiotensin converting enzyme angioedema. 844 May 68

Urticaria and angioedema may be elicited by a considerable number of drugs, particularly nonsteroidal antiinflammatory drugs, angiotensin converting enzyme inhibitors, radiocontrast media and antibiotics. Pathogenic mechanisms involved include pseudoallergy, idiosyncrasy and IgE-mediated hypersensitivity, occasionally also IgG antibodies. In this survey the common problems which still lack established diagnostic in vitro tests such as pseudoallergic reactions to analgesic drugs and idiosyncratic side effects to angiotensin-converting-enzyme inhibitors are presented. In addition some examples of drugs are given where, due to progress in research, instead of a pseudoallergic mechanism an immunological pathogenesis could be demonstrated.
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PMID:Drug-induced urticaria and angioedema caused by non-IgE mediated pathomechanisms. 1058 38

Angiotensin-converting enzyme (ACE) inhibitor associated angioedema was detected in 39 subjects (17%) of 231 consecutive patients examined in the last 5 years at our out-patient clinic for symptoms of angioedema without urticaria. In these patients, angioedema was most commonly localized to the face. The duration of ACE-inhibitor treatment at the onset of angioedema ranged from 1 day to 8 years with a median of 6 months. The time elapsed between onset of angioedema and withdrawal of ACE-inhibitor ranged from 1 day to 10 years with a median of 10 months. Delayed diagnosis is explained by the unusual characteristics of this adverse reaction: angioedema may start years after beginning the treatment and then it recurs irregularly. In fact, ACE-inhibitors seem to facilitate angioedema in predisposed subjects, rather than causing it with an allergic or idiosyncratic mechanism. Thus, while Cl-inhibitor levels are usually normal in subjects developing ACE-inhibitor-dependent angioedema, we found that ACE-inhibitors caused angioedema in Cl-inhibitor-deficient patients. Because the main inactivator of bradykinin is kininase II, which is identical with ACE, it is believed that bradykinin mediates ACE-inhibitor-dependent angioedema. We had the possibility to examine the plasma bradykinin levels in one ACE-inhibitor-treated patient during an angioedema attack and we found very high levels, but we did not find an increase of break-down products of high-molecular-weight-kininogen as observed during acute attacks in hereditary angioedema. Bradykinin fell to normal levels during remission after withdrawal of the drug. These observations indicate that in ACE-inhibitor-induced angioedema, contrary to hereditary angioedema, the reduction of bradykinin catabolic rate plays a predominant role.
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PMID:Angioedema due to angiotensin-converting enzyme inhibitors. 1060 20

Congenital C1-inhibitor deficiency, or hereditary angioneurotic edema (HAE), is a rare autosomal dominant disease due to alterations in the C1 inhibitor gene that results in a deficiency of antigenic and/or functional C1-INH. Affected patients are heterozygous, and their deficiency is incomplete, many of them having up to 20% of the normal amount of the inhibitor. The disease is characterised by recurrent, circumscribed, non-pitting, and non-pruritic subepithelial swellings of sudden onset, which fade during the course of 48-72 hours, but can persist up to 1 week. Lesions can be solitary or multiple and primarily involve the extremities, larynx, face, and bowel wall. Bradykinin is believed to be the main, but certainly not the sole, mediator responsible for the bouts of edema in HAE. The diagnosis is suggested by family history, the lack of accompanying pruritus or urticaria, the presence of recurrent gastrointestinal attacks of colics, and episodes of laryngeal edema. Diminished C4 concentrations during symptomatic periods are highly suggestive for the diagnosis. Further laboratory diagnosis depends on demonstrating a deficiency of C1-INH 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. Prophylactic administration of either attenuated androgens or protease inhibitors has proved useful in reducing frequency or severity of attacks. Infusions of a vapour-heated C1-INH concentrate are safe and effective means of both preventing and treating attacks. Nevertheless, this treatment is expensive and this extract is not readily available. It is emphasised that administration of angiotensin converting enzyme inhibitors is contraindicated in patients suffering from protease inhibitor deficiency states.
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PMID:Hereditary angioneurotic edema: review of the literature. 1078 4

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.
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PMID:[Angiotensin II type-1 receptor antagonists and diabetes mellitus]. 1145 Jan 65

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

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


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