Perinatal environmental influences on goat's and sheep's milk allergy without cow's milk allergy

are also expressed in sympathetic nerves, whereas histamine activates H3-receptors on sympathetic and sensory nerve endings. The H3receptor is cardioprotective by attenuating release of norepinephrine. An imbalance between these 2p athways affects the release of norepinephrine from cardiac sympathetic nerve during myocardial ischemia and can result in arrhythmias and sudden cardiac death. 8 Another possible explanation of this reaction is the occurrence of cardiac anaphylaxis after activation of the anaphylaxis toxin complement factors C3a and C5a and release of histamine after food or drug stimulation. This mechanism has been implicated in peanut-induced anaphylaxis in mice, although the significance of this in human anaphylaxis has not been demonstrated. A genetic variation in complement activation (complotype) in determining the severity of allergic reactions to peanut was demonstrated in animal studies. However, a study in humans did not demonstrate this genetic association in patients with peanut allergy. 9