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(1) Atopy is common in subjects who experience anaphylaxis, regardless of its origin; (2) crustaceans and nonsteroidal anti-inflammatory drugs are the most common food and medication groups, respectively, thought to cause anaphylaxis; (3) causative agents can be identified for two thirds of the subjects, and recurrent attacks are the rule; and (4) subjects with idiopathic anaphylaxis are more likely to carry epinephrine for self-administration than those with identifiable causes.

We describe nine patients with fat malabsorption in whom a spectrum of vitamin E deficiency was present. Early deficiency was generally asymptomatic, and intermediate deficiency produced some impairment. Ataxia, weakness, reflex changes, impaired vision, and pigment retinopathy were associated with chronic, advanced deficiency. In the last group, delayed central somatosensory conduction and amplitude reduction of the electroretinogram were present. In adults, a severe vitamin E deficiency state existed for more than 5 years before producing measurable neurologic damage. The clinical picture is less homogeneous than previously suggested, and electrophysiologic abnormalities need not predate clinical dysfunction.

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