Allergy and Immunology
Anaphylaxis
Anaphylaxis is a clinical diagnosis: acute onset with skin/mucosal involvement plus respiratory compromise or hypotension, or hypotension after a known allergen. Epinephrine is first-line - IM 0.3–0.5 mg of 1:1000 into the lateral thigh, repeated every 5–15 minutes. Antihistamines and steroids treat skin symptoms only and never replace epinephrine. Observe for biphasic reactions; serum tryptase drawn within a few hours supports the diagnosis but a normal value does not exclude it.
Drug allergy and angioedema
The trap is mislabeling. Vasovagal episodes, isolated GI upset, and family history are not allergy. Most penicillin labels are incorrect and can be removed by history plus skin testing. Immediate IgE reactions (urticaria, wheeze) differ from delayed T-cell reactions (maculopapular rash, SJS/TEN, DRESS). Angioedema without urticaria suggests a bradykinin mechanism: ACE-inhibitor angioedema (stop the drug; antihistamines and steroids are ineffective; icatibant or FFP for airway compromise) or hereditary angioedema (low C4, family history, treat with C1-esterase inhibitor or icatibant).
Immunodeficiency
Recurrent sinopulmonary infections in an adult should prompt quantitative immunoglobulins: common variable immunodeficiency shows low IgG with poor vaccine responses and is treated with IVIG. IgA deficiency is usually asymptomatic but risks anaphylaxis to blood products. Terminal complement defects cause recurrent Neisseria infection.
Worked example
A 58-year-old on lisinopril develops tongue swelling over two hours with no hives, wheeze, or hypotension. This is bradykinin-mediated angioedema: stop the ACE inhibitor, secure the airway if needed, and do not expect a steroid or antihistamine response. A trial of icatibant is reasonable; recurrence risk persists for weeks after withdrawal.