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Background: Anaphylaxis after Hymenoptera sting has been described in patients with mastocytosis. Venom immunotherapy (VIT) is a safe and effective way to treat patients with Hymenoptera anaphylaxis, but few studies have addressed its usefulness in patients with systemic mastocytosis., Objective: To study the effectiveness and safety of VIT in patients with systemic mastocytosis having anaphylaxis after Hymenoptera sting., Methods: A total of 21 mastocytosis patients-4 women (19%) and 17 men (81%) with a median age of 50 years (range, 29-74 years)-with Hymenoptera sting anaphylaxis who were treated with VIT and followed for a median of 52 months (range, 2-250 months) were studied., Results: In 18 of 21 patients-16 of them lacking skin involvement-anaphylaxis was the presenting symptom. Six patients (29%) experienced adverse reactions during VIT, 3 during initiation and 3 during maintenance. Twelve patients (57%) were resting while undergoing VIT; 9 (75%) presented local reactions and 3 (25%) systemic reactions, 1 of which required intubation. The Hymenoptera specific IgE decreased from 4.15 kU/L (range, 0.44-100 kU/L) before immunotherapy to 1.2 kU/L (range, 0.34-69.4 kU/L) after 4 years (P < .003)., Conclusion: Venom immunotherapy is effective to treat IgE-mediated Hymenoptera anaphylaxis in patients with mastocytosis. Its use is recommended despite a relatively high risk of adverse reactions during the build-up phase because it provides protection from anaphylaxis in around 3/4 of the patients.

Mastocytosis consists of a group of disorders characterized by a pathologicincrease in mast cells in tissues including skin, bone marrow, liver, spleen, andlymph nodes. Mastocytosis is a rare disease and general practitioners have limited exposure to its clinical manifestations, diagnosis, classification, and management. Moreover a complete and clear review in this field is not easy founded. Diagnosis of mastocytosis is suspected on clinical grounds and is established by histopathologic examination of involved tissues such as skin and bone marrow. The most common clinical sign of mastocytosis is the presence of typical skin lesions of urticaria pigmentosa. Most patients experience symptoms related to mast cell mediator release, and prevention of the effects of these mediators on tissues constitutes the major therapeutic goal in the management of mastocytosis. Despite recent advances in knowledge about the pathophysiology, diagnosis, and classification of mastocytosis, a curative treatment for mastocytosis does not now exist; furthermore mastocytosis is a chronic diseases with different severity grades but in all of them with an important negative impact on quality of live of patients. Management of patients within all categories of mastocytosis includes: 1. A careful counselling of patients (parents in paediatric cases) and care providers. 2. Avoidance of factors triggering acute mediator release. 3. Treatment of acute mast cell mediator release. 4. Treatment of chronic mast cell mediator release, and if indicated. 5. An attempt to treat organ infiltration by mast cells. The goal of this review is to provide a practical guide focus on diagnostic criteria for the different treatment options currently available and their management.

Introduction: Chronic mesenteric ischemia (CMI) is an uncommon disorder. Traditional treatment consists of open surgical (OS) revascularization. We report a case of CMI treated with percutaneous angioplasty and stenting., Case Report: A 77-year-old-woman reported a history of postprandial abdominal pain, weight loss, asthenia, and anorexia. On physical examination, the only relevant sign was systolic murmur. Oral panendoscopy showed chronic atrophic gastritis and patchy intestinal metaplasia with Helicobacter pylori colonization; rectal sigmoidoscopy showed colonic diverticula. Abdominal ultrasound color-flow imaging confirmed superior mesenteric artery (SMA) stenosis > 70%. Angiography confirmed proximal SMA subocclusion and celiac trunk stenosis of 50%. Percutaneous angioplasty and stenting were carried out. The patient made an immediate recovery and remains without postprandial pain., Discussion: CMI due to atherosclerotic occlusive disease was first reported in 1936 and is a relatively uncommon disorder. This entity usually occurs in patients over 60 years of age with other atherosclerotic symptoms. CMI presents with postprandial abdominal pain, anorexia due to <>, and weight loss. Despite high perioperative morbidity and mortality rates, OS revascularization has traditionally been the treatment of choice. The most frequent indications include pain relief, improvement of nutritional status, and prevention of intestinal infarction. Endovascular therapy seems to be a valid alternative, mainly in high-risk patients, with good immediate and medium-term results.

Allergic reactions to beta-lactam antibiotics have been reported frequently and may occur because of sensitization to unique haptens or to determinants shared with other drugs. A woman who received 1 tablet of amoxicillin-clavulanic acid developed wheals and flares although she had previously tolerated the same preparation well. Levels of specific immunoglobulin (Ig) E to penicillin V, penicillin G, amoxicillin, and ampicillin were undetectable. Skin tests to amoxicillin, penicillin major determinant and minor determinant mixture were negative. The patient tolerated oral challenge with 500 mg of amoxicillin but developed wheals and flares when challenged with amoxicillin-clavulanic acid 500/125 mg. A histamine release test was negative with amoxicillin but positive with the amoxicillin-clavulanic acid and clavulanic acid. A prick test to the combination was positive. Specific IgE to penicillin V later became positive while remaining negative to other beta-lactams. No inhibition was obtained using penicillin V against clavulanic acid and amoxicillin but was complete when penicillin V was used in the solid-phase and as the inhibitor. No cross-reactivity was proven between these sensitizations.

H1-antihistamines are commonly used drugs, and probably the most frequently used for allergic diseases. They are pharmacologic inverse agonists of histamine at H1 receptor sites and try to shift the equilibrium of this receptor toward the inactive state, preventing H1 response. A wide variety of adverse effects have been attributed to antihistamines, and they can exceptionally induce skin reactions. We report the case of a patient with several episodes of urticaria induced by different families of antihistamines - piperazines and piperidines. We performed skin prick tests (SPT), patch tests and oral challenges to different antihistamines. We found positive SPT to some antihistamines, and positive oral challenge in others with negative SPT. The route of sensitization remained unclear, and our patient could not finally tolerate any antihistamine after the oral challenges we performed. We support the hypothesis that antihistamines may shift the H1 histamine receptor to the active conformation instead of the inactive conformation, prompting adverse reactions after dosing. This is the first report of urticaria induced by different antihistamines in the same patient with positive SPT to several others.