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Angioedema urticaria [keywords]
- [Use of antihistamines in a physician's clinical practice]. [English Abstract, Journal Article]
- Ter Arkh 2014; 86(8):106-9.
Histamine that belongs to one of the most important mediators involved in the regulation of the body's vital functions plays a great role in the pathogenesis of different diseases. Histamine is released during inflammatory and allergic reactions, anaphylactic and anaphylactoid shock, pseudoallergic reactions, and others. Acting through histamine receptors, it leads to increased intracellular concentration of cyclic guanosine monophosphate, enhanced chemotaxis of eosinophils and neutrophils, production of prostaglandins and thromboxane B, suppressed synthesis of lymphokines, etc. and causes contraction of smooth muscles of particularly the bronchi and intestine, dilation of vessels and their increased permeability, mucus hypersecretion in the upper airways, lower blood pressure, angioedema and itch, etc. In this connection, antihistamines that block histamine-induced reactions in various ways: by inhibiting its biosynthesis, enhancing its neutralization, blocking the access to receptors, and suppressing the release from mast cells, occupy a prominent place in clinical practice. The review covers the classification, main mechanisms of pharmacological action, and indications for the use of antihistamines that not only have the well-known antihistamine properties, but have also a broad spectrum of anti-inflammatory activity. There are data on the benefits of a group of antihistamines, the quinuclidine derivatives (quifenadine, sequifenadine) that were designed by Academician M.D. Mashkovsky and are one of the first examples of designing new classes of multifunctional non-sedating antihistamines, which combines a high selective activity to block histamine type 1 receptors and an ability to block serotonin and to break down histamine directly in tissues.
- Therapeutic imaging window of cerebral infarction revealed by multisequence magnetic resonance imaging: An animal and clinical study. [Journal Article]
- Neural Regen Res 2012 Nov 5; 7(31):2446-55.
In this study, we established a Wistar rat model of right middle cerebral artery occlusion and observed pathological imaging changes (T2-weighted imaging [T2WI], T2FLAIR, and diffusion-weighted imaging [DWI]) following cerebral infarction. The pathological changes were divided into three phases: early cerebral infarction, middle cerebral infarction, and late cerebral infarction. In the early cerebral infarction phase (less than 2 hours post-infarction), there was evidence of intracellular edema, which improved after reperfusion. This improvement was defined as the ischemic penumbra. In this phase, a high DWI signal and a low apparent diffusion coefficient were observed in the right basal ganglia region. By contrast, there were no abnormal T2WI and T2FLAIR signals. For the middle cerebral infarction phase (2-4 hours post-infarction), a mixed edema was observed. After reperfusion, there was a mild improvement in cell edema, while the angioedema became more serious. A high DWI signal and a low apparent diffusion coefficient signal were observed, and some rats showed high T2WI and T2FLAIR signals. For the late cerebral infarction phase (4-6 hours post-infarction), significant angioedema was visible in the infarction site. After reperfusion, there was a significant increase in angioedema, while there was evidence of hemorrhage and necrosis. A mixed signal was observed on DWI, while a high apparent diffusion coefficient signal, a high T2WI signal, and a high T2FLAIR signal were also observed. All 86 cerebral infarction patients were subjected to T2WI, T2FLAIR, and DWI. MRI results of clinic data similar to the early infarction phase of animal experiments were found in 51 patients, for which 10 patients (10/51) had an onset time greater than 6 hours. A total of 35 patients had MRI results similar to the middle and late infarction phase of animal experiments, of which eight patients (8/35) had an onset time less than 6 hours. These data suggest that defining the "therapeutic time window" as the time 6 hours after infarction may not be suitable for all patients. Integrated application of MRI sequences including T2WI, T2FLAIR, DW-MRI, and apparent diffusion coefficient mapping should be used to examine the ischemic penumbra, which may provide valuable information for identifying the "therapeutic time window".
- Icatibant in the treatment of Angiotensin-converting enzyme inhibitor-induced angioedema. [Journal Article]
- Case Rep Crit Care 2014.:864815.
We describe the case of a 75-year-old woman who presented with massive tongue and lip swelling secondary to angiotensin-converting enzyme inhibitor-induced angioedema. An awake fibre-optic intubation was performed because of impending airway obstruction. As there was no improvement in symptoms after 72 hours, the selective bradykinin B2 receptor antagonist icatibant (Firazyr) was administered and the patient's trachea was successfully extubated 36 hours later. To our knowledge this is the first documented case of icatibant being used for the treatment of angiotensin-converting enzyme inhibitor-induced angioedema in the United Kingdom and represents a novel therapeutic option in its management.
- Drug-induced visceral angioedema. [Journal Article, Review]
- J Community Hosp Intern Med Perspect 2014; 4(4)
Angioedema associated with angiotensin converting enzyme inhibitors (ACEIs) is due to the accumulation of bradykinin and its metabolites. Angiotensin receptor blockers (ARBs) produce anti-hypertensive effects by blocking the angiotensin II AT1 receptor action; hence bradykinin-related side effects are not expected. However, we notice the occurrence of ARB-induced angioedema as not a very rare side effect. Visceral drug-induced angioedema has been reported with ACEIs, not with ARBs. This underlying review will help educate readers on the pathophysiology and recent guidelines pertaining to ACEI- and ARB-induced visceral angioedema.
- Progestins are Efficient Agents in Estrogen-sensitive Nonhistaminic Angioedema. [Letter]
- Am J Med 2014 Oct; 127(10):e7.
- Perioperative Management of Tooth Extractions for a Patient With Hereditary Angioedema. [JOURNAL ARTICLE]
- J Oral Maxillofac Surg 2014 Aug 27.
Hereditary angioedema (HAE) is a rare genetic disorder that causes a deficiency in or dysfunction of C1 esterase inhibitor (C1-INH) and is clinically characterized by sudden and recurrent attacks of angioedema. Although almost any part of the body can be affected, HAE is of greatest concern and can be life-threatening when the upper airway is involved, particularly the larynx (laryngeal attack). HAE attacks can be triggered by physical or psychological stress or can arise spontaneously without any apparent trigger. Dental treatments and routine oral surgical procedures, such as tooth extraction, abound with factors that can trigger an attack of HAE. Indeed, several cases of death resulting from HAE attacks have been reported after such procedures. Therefore, patients with HAE are of special concern in dentistry and require precautionary preparations before treatment. This report describes the successful management of tooth extractions in a patient with HAE who was at high risk of an HAE-induced laryngeal attack.
- Quality of life in patients with hereditary angioedema receiving therapy for routine prevention of attacks. [JOURNAL ARTICLE]
- Allergy Asthma Proc 2014 Sep; 35(5):371-376.
Patients with hereditary angioedema (HAE) have impaired health-related quality of life (HRQoL), but the effect of preventative treatment strategies on HRQoL has not been evaluated. This study was designed to evaluate the effect of routine prevention therapy with nanofiltered C1 inhibitor (C1 INH-nf; human) on the HRQoL of patients with HAE. Thiry-six-item Short Form (SF-36) Version 1.0 questionnaires were administered at the beginning and end of two 12-week treatment periods in this multicenter, randomized, placebo-controlled, crossover study. Patients (n = 22) received intravenous injections of 1000 U of C1 INH-nf or placebo every 3-4 days for 12 weeks and then crossed over to the other treatment arm for a second 12-week period. Patients could receive open-label C1 INH-nf (1000 U) for the acute treatment of angioedema attacks in either arm of the study. Sixteen patients had evaluable SF-36 data. Mean physical component summary scores (PCSs) were 36.41 at baseline, 37.06 at the end of the placebo period, and 43.92 at the end of the C1 INH-nf period. Mean mental component summary scores (MCSs) were 49.90, 44.98, and 54.00, respectively. Least square mean differences (95% confidence intervals) between C1 INH-nf and placebo in norm-based SF-36 scores at the end of each treatment period were 6.55 (1.48, 11.62; p = 0.015) for PCS and 8.70 (1.67, 15.72; p = 0.019) for MCS. In a clinical trial setting, patients with HAE had significantly better HRQoL after 12 weeks of C1 INH-nf for routine prevention compared with acute treatment of individual angioedema attacks in the absence of routine prevention while on placebo. This study was a part of the clinical trial NCT01005888 registered in www.clinicaltrials.gov.
- Prognostic factors in outcome of angioedema in the emergency department. [JOURNAL ARTICLE]
- Allergy Asthma Proc 2014 Sep; 35(5):362-370.
Angioedema is a transient, localized swelling caused by two distinct mechanisms, mediated by histamine and bradykinin, respectively, although a proportion of cases remain idiopathic. Studies that characterize undifferentiated angioedema presenting in emergency departments (EDs) are limited. This study investigates the presentation patterns of undifferentiated angioedema in the ED based on the presumed mechanism of swelling. Medical records from all ED visits to two tertiary care hospitals from July 2007 to March 2012 were electronically reviewed. Records with documented visible swelling on general inspection and/or fiberoptic laryngoscopy and a diagnostic code for anaphylactic shock, angioneurotic edema, allergy unspecified, defects in the complement system, or unspecified drug adverse effects were included. Demographic, clinical, and outcome data were collected via a standardized form. Data were analyzed descriptively, including frequencies and percentages for categorical data and means and SDs for continuous data. Predictors for admission were identified using multivariate logistic regression models. ED records from 527 visits for angioedema by 455 patients were included in the study. Annual rate of angioedema was 1 per 1000 ED visits. Urticaria was associated with peripheral (p = 0.008) and lip angioedema (p = 0.001), and the absence of urticaria correlated with tongue angioedema (p = 0.001) and trended toward correlation with pharyngeal angioedema (p = 0.056). Significant predictors of admission included nonsteroidal anti-inflammatory drug-induced angioedema (odds ratio [OR], 15.3), epinephrine treatment (OR, 8.34), hypotension (OR, 15.7), multiple-site angioedema (OR, 4.25), and pharyngeal (OR, 1.23) and tongue angioedema (OR, 4.62). Concomitant urticaria was associated with a significant longer stay in the ED (p < 0.001). The presence of urticaria correlated with the location of angioedema, need for airway management, length of ED visit, and recurrence. A detailed drug and family history, screening blood work for C1 esterase inhibitor deficiency when indicated, and prompt management of angioedema based on presumed mechanism of swelling are crucial steps in managing undifferentiated angioedema in ED.