Today for AM report, we discussed a case of a middle-aged gentleman who presented with monocular blurry vision and was found to have ocular syphilis (see photo below). However to complicate matters, he had a reported allergy to penicillin, describing a potential prior anaphylaxis episode. Fortunately, we had our amazing allergy & immunology fellow (and UCSD IM alum!) Dr. Galant-Swafford present to discuss the approach to taking an allergy history, as well as the different methods for testing and treatment patients with reported PCN allergy! Ultimately, our patient underwent PCN desensitization in the ICU and was treated for a full 14 day course with IV PCN. Thank you Dr. Galant-Swafford for your expertise and excellent discussion points!
- There are many components to taking a drug history, but for PCN, it is especially important to determine if there was an episode of anaphylaxis in the past and to distinguish between immediate and delayed hypersensitivity reactions
- Penicillin skin testing and oral challenge can be appropriate for low risk patients to rule-out an IgE-mediated reaction (and take the allergy off their chart)
- If there are no alternative medication options and suspicion for a true IgE-mediated reaction is high enough (e.g. our patient), then desensitization in the ICU is warranted
here’s the link: https://www.youtube.com/watch?v=lf98UNScYh4
This morning, the inaugural Stephen Wasserman Lecture was given by Dr. Frank Austen. Dr. Austen began by recounting his experiences in the Stephen Wasserman lab where a cohort of post-docs and trainees then went to began their own prolific laboratories replicating the dynamic nature of the Wasserman lab.
Today’s presentation focused on highlighting the work that has led to the understanding of mast cell diversity and heterogeneity–work that has spanned several decades. Dr. Frank Austen highlighted several key studies that underscored differences in lineage development, variety of localization of mast cell progenitors and differences in granulation patterns of mature mast cells. Dr. Austen also highlighted that the hematopoietic lineage development of tissue mast cells is unique compared to other myeloid-derived cells because its early lineage progenitors have been found to leave the bone marrow to enter the circulation. These immature lineage mast cells immediately undergo transendothelial recruitment into peripheral tissues wherein the appearance of secretory granules with a particular protease phenotype is regulated by the peripheral tissue. Altogether these findings suggest dual roles of connective tissue mast cells (CTMCs) and mucosal mast cell (MMC) populations, based on distributions of where these populations reside within a tissue, dependence on T-cells, and lifespan.
Thank you to Dr. Austen for providing a fantastic overview of generations of work in this field and for a fantastic Grand Rounds presentation!
Dr. Fairfield presented a patient with systemic mastocytosis and syncope this morning. Even though the patient’s flushing, swelling, and rash fit a classic “explosive mast cell degranulation” episode, the team pursued a broad differential and excluded the cardiac etiologies with the highest potential for mortality in syncopal patients. Thank you also to Dr. Grobman for a great breakdown of systemic mastocytosis and its treatment. Avoid that anchoring bias friends!
Syncopal algorithm citation:
LLOYD A. RUNSER, MD, MPH, ROBERT L. GAUER, MD, and ALEX HOUSER, DO, Womack Army Medical Center, Fort Bragg, North Carolina. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017 Mar 1;95(5):303-312B.
There is no excerpt because this is a protected post.
This morning our future ID fellow, Sydney Ramirez, presented two cases of angioedema. One patient was in her 50s, experienced associated urticaria, and was responsive to steroids, anti-histamines, and epinephrine. The second patient was in her teens, had a family member with similar issues and was unresponsive to epinephrine and steroids during acute attacks. Dr. Zuraw, EXPERT in angioedema, explained angioedema can be mediated by histamine (IgE mediated v. direct mast cell activation v. immunologic/idiopathic) and by bradykinin (problem with enzymes that break down bradykinin v. dysfunction/deficiency in C1 esterase inhibitor v. antibodies to C1 esterase inhibitor). History and clinical picture is important in differentiating the different types! Key Points: 1. “Histamine responsive” is a term you can use only when a patient has proven to be responsive to high doses antihistamines in the prophylactic setting (i.e. the the number of attacks is decreased). You cannot determine this in the acute setting! 2. There are two main types of angioedema:
Happy Thursday! Today, Dr. Amie Nguyen, one of our AMAZING PGY3’s and soon-to-be-allergy-immunology fellow, presented a case of a young male presenting with chronic, intermittent, progressive, esophageal dysphagia to solids. He was ultimately diagnosed with eosinophilic esophagitis (EoE). We were lucky to have one of our phenomenal GI fellows, Dr. Bobby Klapheke, present to be our expert discussant! We were introduced to EoE Edward, who fits all of the classic features of EoE: A young (20-30 y/o) male with history of atopic dermatitis, asthma, and allergies who has intermittent esophageal dysphagia to solids, found to have ≥ 15 eosinophils/HPF and “feline esophagus” (presence of stacked rings) on esophageal biopsy. Remember that EoE and food allergies are closely intertwined, so ALL patients with EoE should undergo allergy testing!
On Wednesday, Jessica Galant-Swafford (future Allergy and Immunology fellow) presented a case of possible Xolair anaphylaxis. Xolair, or omalizumab, is an antibody to free IgE and is FDA approved for severe persistent allergic asthma and chronic idiopathic urticaria, though it is sometimes used for ABPA as well. There is no clear consensus for the mechanism of anaphylaxis to Xolair and it can present with any combo of angioedema, bronchospasm, hypotension, syncope and urticaria, usually occurring within 2-4 hours after infusion. Lastly, remember that this is RARE (0.1%).
This morning, Dr. Sandra Christiansen, from our department of Allergy and Immunology presented a fantastic grand rounds entitled, “Evaluation and treatment of Aspirin Exacerbated Respiratory Disease (AERD).” She began by presenting a typical case of AERD. Symptoms often begin after a viral upper respiratory infection–more specifically, it feels like the URI lasts for weeks to months. The classic quatrad includes: asthma, sinusitis, aspirin sensitivity, and nasal polyps. The latter, nasal polyps, are profound and highly characteristic of AERD. Other symptoms include GI distress and skin flushing. Aspirin sensitivity was first recognized in the early 20th century, shortly after Aspirin was synthesized. Despite an estimated 1.3 million cases in the USA, it likely remains vastly under-diagnosed. Patients with AERD often suffer significantly. They experience prolonged sinus congestion, loss of smell (which is quite distressing), periodic courses of systemic glucocorticoids, and many sinus surgeries. Treatment can be life-changing. Patients are able to stop systemic glucocorticoids, regain their sense of smell, reduce the number