Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Angioedema urticaria [keywords]
- A critical appraisal of omalizumab as a therapeutic option for chronic refractory urticaria/angioedema. [JOURNAL ARTICLE]
- Ann Allergy Asthma Immunol 2014 Feb 28.
- C-reactive protein levels in Hereditary Angioedema. [JOURNAL ARTICLE]
- Clin Exp Immunol 2014 Mar 4.
Hereditary Angioedema (HAE) patients experience recurrent episodes of angioedema attacks that can be painful, disfiguring and even life-threatening. The disorder results from a mutation in the gene that controls the synthesis of C1-inhibitor (C1INH). C1INH is a major regulator of activation of the contact system. It is often assumed that attacks results from uncontrolled, local activation of the contact system with subsequent formation of bradykinin.To evaluate involvement of inflammatory reactions in HAE, we analyzed C-reactive protein (CRP) levels before, during, and after HAE attacks.HAE patients included in a clinical database of recombinant human C1- inhibitor (rhC1INH) studies were evaluated. For the current study we analyzed CRP levels when patients were asymptomatic, during a clinical attack and in a follow up period, and correlated these with the clinical manifestations of the attack.Data from 68 HAE patients were analyzed and included CRP levels at 273 occasions. While asymptomatic, 20% of the patients analyzed had increased CRP. At the onset of the attack (p=0.049) and over the next 24 hours CRP rose significantly (p=.002) in patients with an abdominal location, and post-attack levels were significantly higher in these patients than in patients with attacks at other locations (p=.034).CRP levels are elevated in a substantial proportion of asymptomatic HAE patients. Levels of CRP significantly increase during an abdominal attack. These data suggest low-grade systemic inflammatory reactions in HAE patients as well as a triggering event for attacks that starts prior to symptom onset.
- Cross-reactivity to Acetaminophen and Celecoxib According to the Type of Nonsteroidal Anti-inflammatory Drug Hypersensitivity. [Journal Article]
- Allergy Asthma Immunol Res 2014 Mar; 6(2):156-62.
Identification of tolerable alternative analgesics is crucial for management in nonsteroidal anti-inflammatory drug (NSAID)-sensitive patients. We investigated cross-reactivity of acetaminophen and celecoxib according to the type of aspirin/NSAID hypersensitivity and aimed to determine the risk factors for cross-intolerance.We retrospectively reviewed the medical records of patients intolerant to aspirin and NSAIDs who had undergone an acetaminophen and/or celecoxib oral provocation test. Aspirin/NSAID hypersensitivity was classified into 4 types according to a recently proposed classification: aspirin-exacerbated respiratory disease (AERD), aspirin-exacerbated chronic urticaria (AECU), aspirin-induced acute urticaria/angioedema (AIAU), and NSAID-induced blended reaction (NIRD).A total of 180 patients with hypersensitivity to aspirin and NSAIDs were enrolled; 149 acetaminophen provocation test results and 145 celecoxib provocation test results were analyzed. The overall cross-reaction rates to acetaminophen and celecoxib were 24.8% and 10.3%, respectively. There was a significant difference in the cross-reactivity to acetaminophen according to the type of NSAID hypersensitivity. Cross-reactivity to acetaminophen was highest in the AECU group (43.9%), followed by the AERD (33.3%), NIBR (16.7%), and AIAU (12.5%) groups. Underlying chronic urticaria was more prevalent in patients with cross-intolerance to both acetaminophen (P=0.001) and celecoxib (P=0.033). Intolerance to acetaminophen was associated with intolerance to celecoxib (P<0.001).Acetaminophen and celecoxib may induce adverse reactions in a non-negligible portion of aspirin/NSAID-sensitive patients. Physicians should be aware of the possible cross-reactions of these alternative drugs and consider an oral challenge test to confirm their tolerability.
- [Urticaria: Diagnosis and treatment.] [JOURNAL ARTICLE]
- Rev Med Interne 2014 Feb 25.
Urticaria is a common inflammatory skin disease. It is clinically defined as the occurrence of transient papular skin and/or mucosal lesions or subcutaneous lesions called angioedema. Chronic urticaria is defined as a clinical course over more than 6weeks. Different clinical forms of urticaria can coexist in the same patient. Urticaria results of mast cell activation. The diagnosis of urticaria is based on clinical examination. An allergic etiology for acute urticaria, although rare, is always to find and remove. Chronic urticaria is not allergic. Diagnosis is based on questioning and a careful clinical examination to rule out differential diagnoses. Few diagnostic tests are necessary for diagnosis and management, and are especially useful in case of doubtful diagnosis. The treatment of urticaria is symptomatic and based on anti-H1 second generation antihistamines as first-line therapy. In some chronic urticarial, antihistamines up dosing may be necessary. In the majority of patients, this treatment is sufficient to control chronic urticaria. In case of antihistamines failure, other treatment particularly immunomodulatory treatments can be offered in specialized departments.
- Assessment of Interleukins IL-4, IL-6, IL-8, IL-10 in Acute Urticaria. [Journal Article]
- J Clin Med Res 2014 Apr; 6(2):133-7.
Urticaria is a skin disease that affects approximately 5% of the general population and manifests itself, not only as an acute but also as a chronic disease. The etiology of the disease varies as well as its clinical manifestations which extend from the presence of urticarial hives to the potentially mortal angioedema. There is a great interest to the disease not only due to its special clinical manifestation but also due to its pathogenetic mechanism. New data in the medical bibliography support the participation of interleukins (ILs) in the pathophysiology of urticaria. The aim of the study is to contribute in the comprehension of possible participation of certain ILs in the pathogenesis of acute urticaria.Our study concerns four ILs, IL-4, IL-6, IL-8 and IL-10, simultaneously and their quantitative changes during the acute phase of urticaria as well as 2 weeks after drug administration. Moreover, ILs levels of patients were compared with those of matched healthy controls. All measurements have been done by the ELISA method. The statistical analysis was done by SPSS.The results present increased levels (in 51 patients vs. 22 matched healthy controls) of all four ILs during the acute phase. Especially for IL-4 this increase was statistically very significant (P < 0.001). Statistically marginally significant decrease was also observed for IL-10 concentrations (P < 0.059), for the two blood samples (acute phase and 2 weeks later).It is suggested by the present study that certain ILs might play an important role in the pathogenetic mechanism of urticaria. IL-4 and IL-10 participation seems to be relatively more significant. Possibly, ILs, liberated by mast cells, induce an influx of leukocytes in the dermis, therefore participating in the development of acute urticaria inflammation.
- Disease spectrum in patients with elevated serum tryptase levels. [JOURNAL ARTICLE]
- Australas J Dermatol 2014 Feb 19.
Elevated serum tryptase levels can be a sign of mastocytosis, which is a rare disease associated with systemic and/or skin manifestations.To investigate patients with elevated tryptase levels in regard to their underlying diseases, and to determine whether increased tryptase can be used as a diagnostic marker for underlying mastocytosis.In a retrospective study the data of 96 patients with serum tryptase levels higher than 15 μg/L were systematically analysed. In 48 patients control investigations for baseline tryptase were performed.Fifty-three of the 96 patients had tryptase levels ≥20 μg/L. A mere 16% of the 96 patients suffered from mastocytosis and had the highest tryptase levels (P < 0.001). The remaining patients had anaphylaxis (36%), urticaria and angioedema (26%), local reactions to insect bites (4%), drug reactions (3%), or miscellaneous diagnoses (15%). Only 16 of these had acute symptoms at tryptase investigation. In all, 48 patients had a follow up; in 7/48 patients with acute symptoms normal tryptase levels were seen at control investigations, but 41/48 (85%) patients showed continuously elevated tryptase levels >15 μg/L and in 30 patients (62%) even values >20 μg/L; 11 of these patients had anaphylaxis, five urticaria, five other diagnoses and nine patients mastocytosis.More than 50% of patients with non-mastocytosis such as urticaria and angioedema, drug or anaphylactic reactions repeatedly had tryptase levels higher than 20 μg/L. Since baseline tryptase >20 μg/L is a minor criterion for mastocytosis, these patients should be inspected for skin lesions of mastocytosis and receive a diagnostic body work-up for systemic mastocytosis including a bone marrow biopsy.
- Kinin Receptors in Vascular Biology and Pathology. [JOURNAL ARTICLE]
- Curr Vasc Pharmacol 2014 Feb 26.
Endogenous kinins are important vasoactive peptides whose effects are mediated by two G-Protein-coupled receptors (R), named B2R (constitutive) and B1R (inducible). They are involved in vascular homeostasis, ischemic pre- and post- conditioning, but also in cardiovascular diseases. They contribute to the therapeutic effects of angiotensin-1 converting enzyme inhibitors (ACEI) and angiotensin AT1 receptor blockers. Benefits derive primarily from vasodilatory, antiproliferative, antihypertrophic, antifibrotic, antithrombic and antioxidant properties, which are associated with the release of endothelial factors such as nitric oxide, prostacyclin and tissue plasminogen activator. Uncontrolled production of kinins or the inhibition of their metabolism may lead to unwanted pro-inflammatory side effects. Thus, B2R antagonism is salutary in angioedema, septic shock, stroke, and Chagas vasculopathy. B1R is virtually absent in healthy tissues, yet this receptor is induced by the cytokine pathway and the oxidative stress via the transcriptional nuclear factor NF-κB. The B1R may play a compensatory role for the lack of B2R, and its up-regulation during tissue damage may be a useful mechanism of host defense. Activation of both receptors may be benefit, notably in neovascularisation, angiogenesis, heart ischemia and diabetic nephropathy. At the same time, B1R is a potent activator of inducible nitric oxide and NADPH oxidase, which are associated with vascular inflammation, increased permeability, insulin resistance, endothelial dysfunction and diabetic complications. The dual beneficial and deleterious effects of kinin receptors and, particularly B1R, raise an unsettled issue on the therapeutic value of B1R/B2R agonists versus antagonists in cardiovascular diseases. Hence, the Janus-faced of kinin receptors needs to be seriously addressed in the upcoming clinical trials for each pathological setting.
- Escalating Doses of C1 Esterase Inhibitor (CINRYZE) for Prophylaxis in Patients With Hereditary Angioedema. [Journal Article]
- J Allergy Clin Immunol Pract 2014 Jan-Feb; 2(1):77-84.e1.
Nanofiltered C1 inhibitor (human) is approved in the United States for routine prophylaxis of angioedema attacks in patients with hereditary angioedema, a rare disease caused by a deficiency of functional C1 inhibitor.To assess the safety of escalating doses of nanofiltered C1 inhibitor (human) in patients who were not adequately controlled on the indicated dose (1000 U every 3 or 4 days).Eligible patients had >1 attack/month over the 3 months before the trial. Doses were escalated to 1500 U every 3 or 4 days for 12 weeks, at which point, the patients were evaluated. If treatment was successful (≤1 attack/mo) or at the investigator's discretion, the patients entered a 3-month follow-up period. The patients with an average of >1 attack/month were eligible for further escalation to 2000 U and then 2500 U.Twenty patients started at 1500 U; 13 were escalated to 2000 U, and 12 were escalated to 2500 U. Eighteen patients reported adverse events. Two patients reported 4 serious adverse events (cerebral cystic hygroma, laryngeal angioedema attack, anemia, and bile duct stone) that were considered by investigators to be unrelated to treatment. Notably, there were no systemic thrombotic events or discontinuations due to adverse events. Fourteen patients were treated successfully (70%), continued to the follow-up period at the investigator's discretion, or experienced a reduction in attacks of >1.0/month.Dose escalation of nanofiltered C1 inhibitor (human) up to 2500 U was well tolerated and reduced attack frequency in the majority of patients.
- Antibiotic allergies in children and adults: from clinical symptoms to skin testing diagnosis. [Journal Article]
- J Allergy Clin Immunol Pract 2014 Jan-Feb; 2(1):3-12.
Hypersensitivity reactions to β-lactam and non-β-lactam antibiotics are commonly reported. They can be classified as immediate or nonimmediate according to the time interval between the last drug administration and their onset. Immediate reactions occur within 1 hour after the last drug administration and are manifested clinically by urticaria and/or angioedema, rhinitis, bronchospasm, and anaphylactic shock; they may be mediated by specific IgE-antibodies. Nonimmediate reactions occur more than 1 hour after the last drug administration. The most common manifestations are maculopapular exanthems; specific T lymphocytes may be involved in this type of manifestation. The diagnostic evaluation of hypersensitivity reactions to antibiotics is usually complex. The patient's history is fundamental; the allergic examination is based mainly on in vivo tests selected on the basis of the clinical features and the type of reaction, immediate or nonimmediate. Immediate reactions can be assessed by immediate-reading skin tests and, in selected cases, drug provocation tests. Nonimmediate reactions can be assessed by delayed-reading skin tests, patch tests, and drug provocation tests. However, skin tests have been well validated mainly for β-lactams but less for other classes of antibiotics.
- Implantable venous access device associated complications in patients with hereditary angioedema. [Journal Article]
- J Allergy Clin Immunol Pract 2013 Sep-Oct; 1(5):524-5.