Intimate Contact Could Be Dangerous for Your Health.

Purpose: To review evidence of hypersensitivity reactions to allergens and/or pathogens transmitted via intimate contact.

Methods: We reviewed PubMed for publications in English between 1980 and 2018 using the terms allergy, drugs, foods, hypersensitivity, intercourse, kissing, Kounis syndrome, mast cells, and semen.

Findings: In human RELATIONSHIPS, intimate contact can occasionally have disastrous or even fatal consequences because antigens and pathogens can be transmitted via the oral and vaginal mucosa.

Foods, Drugs and Environmental Factors: Novel Kounis Syndrome Offenders.

Kounis syndrome is hypersensitivity coronary disorder induced by various types of environmental exposures, drugs, conditions and stents. Allergic, hypersensitivity, anaphylactic and anaphylactoid reactions are associated with this syndrome. The disorder manifests as coronary spasms, acute myocardial infarction and stent thrombosis and affects the cerebral and mesenteric as well as coronary arteries.

Adverse cardiac events to monoclonal antibodies used for cancer therapy: The risk of Kounis syndrome.

Monoclonal antibodies are currently used in the treatment of neoplastic, hematological, or inflammatory diseases, a practice that is occasionally associated with a variety of systemic and cutaneous adverse events. Cardiac adverse events include cardiomyopathy, ventricular dysfunction, arrhythmias, arrests, and acute coronary syndromes, such as acute myocardial infarction and vasospastic angina pectoris. These events generally follow hypersensitivity reactions including cutaneous erythema, pruritus chills, and precordial pain.

The more allergens an atopic patient is exposed to, the easier and quicker anaphylactic shock and Kounis syndrome appear: Clinical and therapeutic paradoxes.

Kounis syndrome is a condition that combines allergic, hypersensitivity, anaphylactic or anaphylactoid reactions with acute coronary syndromes including vasospastic angina, acute myocardial infarction and stent thrombosis. This syndrome is a ubiquitous disease affecting patients of any age, involving numerous and continuously increasing causes, with broadening clinical manifestations and covering a wide spectrum of mast cell activation disorders. Drugs, environmental exposures and various conditions are the main offenders.

White blood cell counts, leukocyte ratios, and eosinophils as inflammatory markers in patients with coronary artery disease.

Inflammation is a key feature of atherosclerosis and its clinical manifestations. The leukocyte count has emerged as a marker of inflammation that is widely available in clinical practice. Since inflammation plays a key role in atherosclerosis and its end results, discovering new biomarkers of inflammation becomes important in order to help diagnostic accuracy and provide prognostic information about coronary cardiac disease.

Thrombus Formation Patterns in HeartMate II Continuous-Flow Left Ventricular Assist Devices: A Multifactorial Phenomenon Involving Kounis Syndrome?

Metallic devices are increasingly used in contemporary cardiological practice. They include coronary stents, artificial cardiac valves, bioprostheses for transcatheter aortic valve replacement, closure devices for patent foramen ovale and atrial septal defects, pacemakers, defibrillators, and left ventricular assist devices. Metals constitute the main components of these devices.

Stent hypersensitivity and infection in sinus cavities.

Persistent mucosal inflammation, granulation tissue formation, hypersensitivity, and multifactorial infection are newly described complications of retained drug-eluting stents from endoscopic sinus surgery for refractory rhinosinusitis. In an important report published in Allergy and Rhinology, a 45-year-old male patient suffering from recalcitrant chronic rhinosinusitis underwent functional endoscopic sinus surgery and was found, for the first time, to have steroid-eluting catheters that were inadvertently left in the ethmoid and frontal sinuses. The retained catheters had caused persistent mucosal inflammation and formation of granulation tissue denoting hypersensitivity reaction.

Anaphylactic Shock: Kounis Hypersensitivity-Associated Syndrome Seems to be the Primary Cause.

Experiments have shown that anaphylaxis decreases cardiac output; increases left ventricular end diastolic pressure; induces severe early acute increase in respiratory resistance with pulmonary interstitial edema; and decreases splanchnic, cerebral, and myocardial blood flow more than what would be expected from severe arterial dilation and hypotension. This is attributed to the constrictive action of inflammatory mediators released during anaphylactic shock. Inflammatory mediators such as histamine, neutral proteases, arachidonic acid products, platelet-activating factor (PAF), and a variety of cytokines and chemokines constitute the pathophysiologic basis of Kounis hypersensitivity-associated acute coronary syndrome.