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1.  Angioedema suppressed by a combination of anti-histamine and leukotriene modifier 
Rationale
Angioedema without co-existent urticaria is due to a limited number of causes, including hereditary and acquired C1 esterase inhibitor deficiency, drug-induced angioedema or idiopathic histaminergic or non-histaminergic angioedema. We describe a cohort of patients with recurrent angioedema whose clinical features and response to medications are distinct from the causes above.
Methods
Patients were accrued retrospectively from an academic allergy practice between 2007 and 2014. After institutional research ethics board approval, patients’ charts were reviewed and demographic, clinical and laboratory data were extracted.
Results
A total of 11 patients were recruited. The mean age at presentation was 54.9 years (range 19–70 years) and 6 of 11 were male. The mean number of episodes per year was 18.7 (range 2–60) and mean duration of episodes was 22.4 h (range 4–96). About half of episodes (52%) began overnight. Areas of involvement were lips (73%), tongue (64%), eyelids (18%), feet (36%) and hands (27%). None of the patients had low C3, C4, or CH50; none had significantly positive ANA; C1 esterase inhibitor level and function and C1q were normal in all patients tested. In these 11 patients, complete suppression of recurrences by the combination of cetirizine 20 mg daily and montelukast 10 mg daily was reported by 9 (82%) of patients; whereas 2 (18%) of patients had a partial response to this combination of medications.
Conclusions
Herein, we report a form of angioedema without urticaria, mediated by a combination of histamine and leukotrienes. Clinical, demographic and therapeutic characteristics differentiate this from other recognized causes of angioedema.
doi:10.1186/s13223-017-0201-1
PMCID: PMC5469062
Angioedema; Urticaria; Histaminergic; Non-histaminergic; Anti-histamines; Leukotriene receptor antagonist; Cetirizine; Montelukast
2.  Canadian Society of Allergy and Clinical Immunology annual scientific meeting 2016 
Alsayegh, Mohammad A. | Alshamali, Hanan | Khadada, Mousa | Ciccolini, Amanda | Ellis, Anne K. | Quint, Diana | Powley, William | Lee, Laurie | Fiteih, Yahya | Baksh, Shairaz | Vliagoftis, Harissios | Gerega, Sebastien K. | Millson, Brad | Charland, Katia | Barakat, Stephane | Sun, Xichun | Jimenez, Ricardo | Waserman, Susan | FitzGerald, Mark J. | Hébert, Jacques | Cognet-Sicé, Josiane | Renahan, Kevin E. | Huq, Saiful | Chooniedass, Rishma | Sawyer, Scott | Pasterkamp, Hans | Becker, Allan | Smith, Steven G. | Zhang, Shiyuan | Jayasundara, Kavisha | Tacon, Claire | Simidchiev, Alex | Nadeau, Gilbert | Gunsoy, Necdet | Mullerova, Hana | Albers, Frank | Kim, Young Woong | Shannon, Casey P. | Singh, Amrit | Neighbour, Helen | Larché, Mark | Tebbutt, Scott J. | Klopp, Annika | Vehling, Lorena | Becker, Allan B. | Subbarao, Padmaja | Mandhane, Piushkumar J. | Turvey, Stuart E. | Sears, Malcolm R. | Azad, Meghan B. | Loewen, Keely | Monchka, Barret | Mahmud, Salaheddin M. | Jong, Geert ‘t | Longo, Cristina | Bartlett, Gillian | Ducharme, Francine M. | Schuster, Tibor | MacGibbon, Brenda | Barnett, Tracie | North, Michelle L. | Brook, Jeff | Lee, Elizabeth | Omana, Vanessa | Thiele, Jenny | Steacy, Lisa M. | Evans, Greg | Diamond, Miriam | Sussman, Gordon L. | Amistani, Yann | Abiteboul, Kathy | Tenn, Mark W. | Yang, ChenXi | Carlsten, Christopher | Conway, Edward M. | Mack, Douglas | Othman, Yasmin | Barber, Colin M. | Kalicinsky, Chrystyna | Burke, Andrea E. | Messieh, Mary | Nair, Parameswaran | Che, Chun T. | Douglas, Lindsay | Liem, Joel | Duan, Lucy | Miller, Charlotte | Dupuis, Pascale | Connors, Lori A. | Fein, Michael N. | Shuster, Joseph | Hadi, Hani | Polk, Brooke | Raje, Nikita | Labrosse, Roxane | Bégin, Philippe | Paradis, Louis | Roches, Anne Des | Lacombe-Barrios, Jonathan | Mishra, Sanju | Lacuesta, Gina | Chiasson, Meredith | Haroon, Babar | Robertson, Kara | Issekutz, Thomas | Leddin, Desmond | Couban, Stephen | Connors, Lori | Roos, Adrienne | Kanani, Amin | Chan, Edmond S. | Schellenberg, Robert | Rosenfield, Lana | Cvetkovic, Anna | Woodward, Kevin | Quirt, Jaclyn | Watson, Wade T. A. | Castilho, Edson | Sullivan, Jennifer A. | Temple, Beverley | Martin, Donna | Cook, Victoria E. | Mills, Christopher | Portales-Casamar, Elodie | Fu, Lisa W. | Ho, Alexander | Zaltzman, Jeffrey | Chen, Lucy | Vadas, Peter | Gabrielli, Sofianne | Clarke, Ann | Eisman, Harley | Morris, Judy | Joseph, Lawrence | LaVieille, Sebastien | Ben-Shoshan, Moshe | Graham, François | Barnes, Charles | Portnoy, Jay | Stagg, Vincent | Simons, Elinor | Lefebvre, Diana | Dai, David | Mandhane, Piushkumar | Sears, Malcolm | Tam, Herman | Simons, F. Estelle R. | Alotaibi, Dhaifallah | Dawod, Bassel | Tunis, Matthew C. | Marshall, Jean | Desjardins, Marylin | Béland, Marianne | Lejtenyi, Duncan | Drolet, Jean-Phillipe | Lemire, Martine | Tsoukas, Christos | Noya, Francisco J.D. | Alizadehfar, Reza | McCusker, Christine T. | Mazer, Bruce D. | Maestre-Batlle, Danay | Gunawan, Evelyn | Rider, Christopher F. | Bølling, Anette K. | Pena, Olga M. | Suez, Daniel | Melamed, Isaac | Hussain, Iftikhar | Stein, Mark | Gupta, Sudhir | Paris, Kenneth | Fritsch, Sandor | Bourgeois, Christelle | Leibl, Heinz | McCoy, Barbara | Noel, Martin | Yel, Leman | Scott, Ori | Reid, Brenda | Atkinson, Adelle | Kim, Vy Hong-Diep | Roifman, Chaim M. | Grunebaum, Eyal | AlSelahi, Eiman | Aleman, Fernando | Oberle, Amber | Trus, Mike | Sussman, Gordon | Kanani, Amin S. | Chambenoi, Olivier | Chiva-Razavi, Sima | Grodecki, Savannah | Joshi, Nikhil | Menikefs, Peter | Holt, David | Pun, Teresa | Tworek, Damian | Hanna, Raphael | Heroux, Delia | Rosenberg, Elli | Stiemsma, Leah | Turvey, Stuart | Denburg, Judah | Mill, Christopher | Teoh, Timothy | Zimmer, Preeti | Avinashi, Vishal | Paina, Mihaela | Darwish Hassan, Ahmed A. | Oliveria, John Paul | Olesovsky, Chris | Gauvreau, Gail | Pedder, Linda | Keith, Paul K. | Plunkett, Greg | Bolner, Michelle | Pourshahnazari, Persia | Stark, Donald | Vostretsova, Kateryna | Moses, Andrew | Wakeman, Andrew | Singer, Alexander | Gerstner, Thomas | Abrams, Elissa | Johnson, Sara F. | Woodgate, Roberta L.
doi:10.1186/s13223-017-0192-y
PMCID: PMC5390240
3.  Insights and advances in chronic urticaria: a Canadian perspective 
In the past few years there have been significant advances which have changed the face of chronic urticaria. In this review, we aim to update physicians about clinically relevant advances in the classification, diagnosis and management of chronic urticaria that have occurred in recent years. These include clarification of the terminology used to describe and classify urticaria. We also detail the development and validation of instruments to assess urticaria and understand the impairment on quality-of-life and the morbidity caused by this disease. Additionally, the approach to management of chronic urticaria now focuses on evidence-based use of non-impairing, non-sedating H1-antihistamines given initially in standard doses and if this is not effective, in up to 4-fold doses. For urticaria refractory to H1-antihistamines, omalizumab treatment has emerged as an effective, safe option.
doi:10.1186/s13223-015-0072-2
PMCID: PMC4336710  PMID: 25705232
Chronic urticaria; Diagnosis; Classification; Management; Immunology; Antihistamines; Up-dosing; Omalizumab
4.  A Missed Opportunity 
doi:10.1007/s11606-012-2248-5
PMCID: PMC3631074  PMID: 23150069
medical education;  cognition; problem solving; infectious disease; immunology
5.  Relationship between platelet activating factor acetylhydrolase activity and apolipoprotein B levels in patients with peanut allergy 
Background
Platelet-activating factor (PAF) is a highly potent phospholipid mediator responsible for the life-threatening manifestations of anaphylaxis. PAF acetylhydrolase (PAF-AH) inactivates PAF and protects against severe anaphylaxis whereas deficiency of PAF-AH predisposes to severe or fatal anaphylaxis. Determinants of PAF-AH activity have not been studied in patients with peanut allergy.
Objectives
To determine whether plasma PAF-AH activity in patients with peanut allergy is related to formation of circulating complexes with apolipoprotein B (apoB) the main surface protein on low density lipoprotein particles.
Methods
Plasma PAF-AH activity and apoB concentrations were measured in 63 peanut allergic patients (35 boys, 28 girls, ages 2 – 19 years). ApoB concentration was measured immunoturbidimetrically using goat anti-human apoB. The correlation between PAF-AH activity and apoB concentration was determined.
Results
A positive correlation was found between PAF-AH activity and apoB concentration (r2 = 0.59, P < 0.0001).
Conclusion
In peanut allergic patients, PAF-AH activity strongly correlates with apoB concentration, suggesting the presence of circulating PAF-AH- lipoprotein complexes.
doi:10.1186/1710-1492-10-20
PMCID: PMC4012516  PMID: 24808915
Anaphylaxis; Platelet-activating factor (PAF); PAF-acetylhydrolase (PAF-AH); Low density lipoprotein (LDL); Apolipoprotein B (apoB)
7.  Schnitzler syndrome with cold-induced urticaria 
Background
Schnitzler syndrome encompasses monoclonal gammopathy, urticaria, inflammation, recurrent fever, bone pain and arthralgia, with occasional lymphadenopathy and/or hepatosplenomegaly. It is a rare condition with approximately 100 cases reported in the literature. To our knowledge, this is the first reported case of cold-induced physical urticaria with Schnitzler syndrome.
Main observations
A 43-year-old woman presented to an allergy and immunology clinic with a 7 year history of chronic urticaria, angioedema with anaphylaxis, monoclonal gammopathy and bone pain. Her urticaria was triggered by cooler temperatures and an ice cube test for cold induced urticaria was positive. In spite of aggressive therapies this patient remains symptomatic.
Conclusions
Schnitzler syndrome is under-recognized, particularly variants of the classical description of Schnitzler syndrome. Other diseases, especially those of hematologic origin, should be ruled out. This condition is largely refractory to conventional therapies, although novel treatments, such as interleukin-1 receptor inhibitor, may show promise.
doi:10.3315/jdcr.2010.1060
PMCID: PMC3157821  PMID: 21886751
arthralgia; cold-induced; fever; lymphadenopathy; hepatosplenomegaly; monoclonal gammopathy; Schnitzler syndrome; urticaria
8.  Peanut Allergy: An Overview 
Peanut allergies have been increasing in prevalence in most industrialized countries. Onset is typically in early childhood, with a trend towards earlier ages of presentation. The allergy is lifelong in most affected children, although 15-22% will outgrow their peanut allergy, usually before their teenage years. Manifestations of peanut allergy range from mild to severe, and risk factors predisposing to severe reactions are discussed. However, even in the absence of risk factors, peanut allergic individuals may still experience life-threatening anaphylactic reactions. Approaches to investigation and treatment, patterns of cross-reactivity and possible causes of rising prevalence are discussed.
doi:10.1186/1710-1492-4-4-139
PMCID: PMC2868887  PMID: 20525136
peanut; allergy; anaphylaxis; nuts
9.  Induction of circulating phospholipase A2 by intravenous administration of recombinant human tumour necrosis factor 
Mediators of Inflammation  1992;1(4):235-240.
We have examined the effects of intravenous infusion of recombinant human tumour necrosis factor (rh-TNF) on serum activity of phospholipase A2 (PLA2) in patients with malignancies. Nine patients received a 24 h continuous intravenous infusion ranging from 1.0 × 105 U/m2 to 3.0 × 105 U/m2; 14 patients received a 5 day continuous intravenous infusion ranging from 0.5 × 105 U/m2/day to 3.0 105 U/m2/day. Twenty one of 23 patients responded with marked increases in serum PLA2 activity that were detectable 3 h after the beginning of the rh-TNF infusion and reached maximum levels at 18 h with a mean increase of 16.2-fold. In patients receiving a 5 day rh-TNF infusion, the highest levels of PLA2 were observed after the first day of infusion. Serum PLA2 activity declined continuously to 2.9-fold above baseline at the end of the infusion. A significant correlation was noted between the dose of infused rh-TNF and the maximum increase in PLA2 activity. To our knowledge, this is the first time that an association between intravenous TNF administration and induction of circulating PLA2 in man has been established.
doi:10.1155/S0962935192000358
PMCID: PMC2365345  PMID: 18475466
10.  Preface 
Mediators of Inflammation  1994;3(4):241.
doi:10.1155/S0962935194000347
PMCID: PMC2367048  PMID: 18472949

Results 1-10 (10)