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. Clinical and therapeutic paradoxes concerning Kounis syndrome therapy, pathophysiology, clinical course and causality have been encountered during its clinical course. Drugs that counteract allergy, such as H2-antihistamines, can induce allergy and Kounis syndrome. The more drugs an atopic patient is exposed to, the easier and quicker anaphylaxis and Kounis syndrome can occur. Every anesthetized patient is under the risk of multiple drugs and substances that can induce anaphylactic reaction and Kounis syndrome. The heart and the coronary arteries seem to be the primary target in severe anaphylaxis manifesting as Kounis syndrome. Commercially available adrenaline saves lives in anaphylaxis but it contains as preservative sodium metabisulfite and should be avoided in the sulfite allergic patients. Thus, careful patient past history and consideration for drug side effects and allergy should be taken into account before use. The decision to prescribe a drug where there is a history of previous adverse reactions requires careful assessment of the risks and potential benefits.

Is hypertension a manifestation of the nutcracker phenomenon/syndrome? Case report and brief review of the literature.

Hypertension has been rarely reported in patients with the nutcracker phenomenon/syndrome. We describe a young male adult where a computed tomography angiography provided evidence of left renal vein dilatation, probably due to its compression through the angle between the aorta and the superior mesenteric artery, during the evaluation for secondary hypertension. As there were no other signs for secondary hypertension, we proceeded with a venography of the inferior vena cava and the renal veins that revealed mild anatomical findings compatible with the so called nutcracker phenomenon/syndrome. Blood levels of renin and aldosterone and renocaval pressure gradient from these sites were between normal limits. As there were coexisting anatomical and clinical findings (hypertension), nutcracker syndrome might have been claimed. However, no causal links could be established and these findings should be considered only as a coincidence.