|LETTER TO THE EDITOR
|Year : 2022 | Volume
| Issue : 3 | Page : 429-430
Bee sting-induced central retinal artery occlusion: A new manifestation of Kounis syndrome?
Nicholas G Kounis1, Virginia Mplani2, Ioanna Koniari3
1 Department of Cardiology, University of Patras Medical School, Patras, Greece
2 Intensive Care Unit, University of Patras Medical School, Patras, Greece
3 Department of Cardiology, University Hospital of South Manchester NHS Foundation Trust, Manchester, UK
|Date of Submission||12-Sep-2021|
|Date of Decision||14-Sep-2021|
|Date of Acceptance||27-Sep-2021|
|Date of Web Publication||02-Nov-2022|
Nicholas G Kounis
Department of Cardiology, University of Patras Medical School, Queen Olgas Square, Patras 26221
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kounis NG, Mplani V, Koniari I. Bee sting-induced central retinal artery occlusion: A new manifestation of Kounis syndrome?. Oman J Ophthalmol 2022;15:429-30
|How to cite this URL:|
Kounis NG, Mplani V, Koniari I. Bee sting-induced central retinal artery occlusion: A new manifestation of Kounis syndrome?. Oman J Ophthalmol [serial online] 2022 [cited 2023 Mar 29];15:429-30. Available from: https://www.ojoonline.org/text.asp?2022/15/3/429/360409
To the Editor,
In the interesting report published in Oman J Ophthalmology, a 54-year-old male developed severe anaphylaxis accompanied by reduced vision in the left eye following multiple bee stings on the neck and face. Fundus examination showed retinal ischemic edema, and fundus fluorescein angiogram revealed delayed arm-to-retina time, ischemic macula, and diffuse edema around the foveal avascular zone compatible with central retinal artery occlusion (CRAO). The authors correctly anticipated that a central retinal artery vasospasm, following serial bee stings via the Kounis reaction, was the most likely mechanism of CRAO. Indeed, Kounis syndrome is not only a single-organ disease but also a complex multisystem and multi-organ condition that affects not only the coronary arteries but also the cerebral, peripheral, and mesenteric arteries. The pathophysiologic basis for Kounis syndrome is based on activation of mast cells and other, interacting with mast cells, inflammatory cells. In this cascade, platelets also play a crucial role.
Mast cells can be activated via allergens cross-linking the allergen-specific IgEs bound to high-affinity Fc epsilon receptors. Non-IgE-mediated mast cell degranulation via activation of the complement C1q, C3a C4, C5a, and Factor B, which are called anaphylatoxins, is also involved. The low-affinity Mas-related G protein-coupled receptor X2 (MRGPRX2) may also activate mast cells via non-Fc epsilon receptors. Finally, neuropeptides, including corticotropin-releasing hormone, neurotensin, and substance P via high-affinity receptors, can also activate the mast cells.
Platelet adhesion, activation, and aggregation constitutes the main cause of arterial thrombosis. Several well-known receptors for thromboxane, adenosine diphosphate, and glycoprotein IIb/IIIa as well as receptors for multiple exogenous agonists that contribute to platelet activation, are based on the platelet surface. The latter include receptors for thrombin, serotonin, epinephrine, platelet-activating factor, histamine, as well as FcgRI, FcgRII, FceRI, and FceRII receptors. When these are activated by corresponding mediators released during mast cell degranulation, the result is the Kounis hypersensitivity-associated coronary syndrome.
The cerebral arterial vasculature has been the target of Kounis syndrome on several occasions from various causes. A 41-year-old man developed a fatal right middle cerebral artery territory stroke following an attack by more than 50 bees. Two patients, with mast cell-related disorders, developed transient cerebral ischemic attacks while they had a previous history of chest pain and Kounis syndrome. In a 72-year-old woman, gadolinium-induced anaphylaxis manifesting as Kounis syndrome was complicated with rectosigmoid ischemia and cerebral coma. Recently, another patient of ours, with Kounis syndrome type I variant caused by wasp sting, developed irreversible diffuse hypoxic-ischemic encephalopathy and remained in a vegetative state for 6 months. Another patient with Kounis syndrome type II variant caused by an allergic reaction to amoxicillin-clavulanic acid under general anesthesia was complicated with severe, irreversible ischemic, and fatal encephalopathy. A 55-year-old man suffering from congenital vertebral artery hypoplasis developed lateral meduullary syndrome due to ischemic stroke which was associated with anaphylaxis after eating salad in a restaurant.
Despite that honey bees produce honey and are among the most beneficial creatures that pollinate a third of everything we eat and play a vital role in sustaining the planet's ecosystems, their sting venom named apitoxin (from Latin apis = bee and Greek toxikon = poison) can be dangerous and devastating due to potential allergic and cardiovascular effects.
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Conflicts of interest
There are no conflicts of interest.
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Bee sting-induced acute ischemic stroke: A new manifestation of Kounis syndrome? Ann Indian Acad Neurol 2021;24:118-20. [Full text]
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