To determine whether the incidence of asthma had increased in Rochester, Minnesota, from January 1, 1964 through December 31, 1983, we used a population-based computer-linked medical diagnosis system to identify individual medical records with diagnosis of asthma or other conditions mimicking asthma. All records were reviewed using explicit predetermined diagnostic criteria; we identified 3,622 incident cases of asthma, including definite asthma (n = 1,547), probable asthma (n = 952), and single wheezing episodes (n = 1,123). The annual age- and sex-adjusted incidence of definite + probable asthma rose from 183 per 100,000 in 1964 to 284 per 100,000 in 1983. This rise was entirely accounted for by increased incidence rates in children and adolescents (age range, 1 to 14 yr); incidence rates for infants younger than 1 yr of age and for adults remained constant. For definite + probable asthma cases, the incidence rates for males were higher than for females from infancy through 9 yr of age and for persons older than 50; incidence rates for females were higher than for males from 15 through 49 yr of age. The median age at onset was 3 yr for males and 8 yr for females. We conclude that asthma begins in early childhood, with a higher incidence and earlier onset in males, and that the increase in incidence rates seen from 1964 to 1983 occurred only in children and in adolescents.

A 450-mg dose of TNX-901 significantly and substantially increased the threshold of sensitivity to peanut on oral food challenge from a level equal to approximately half a peanut (178 mg) to one equal to almost nine peanuts (2805 mg), an effect that should translate into protection against most unintended ingestions of peanuts.

Exposure to the aeroallergen A. alternata is a risk factor for respiratory arrest in children and young adults with asthma.

Tryptase, a neutral protease of human mast cells, is a potentially important indicator of mast cell involvement in various clinical conditions. The current study examined the time course of appearance and disappearance of tryptase in the circulation after an anaphylactic event and the stability of both endogenous and exogenous tryptase in terms of freeze-thawing and temperature. The peak level of tryptase after an experimentally induced systemic anaphylactic reaction occurred 1-2 h after the initiating bee sting in each of three subjects, in contrast to histamine levels which peaked at 5-10 min. In some cases elevated levels of tryptase may not be detected during the initial 15-30 min. Tryptase levels then declined under apparent first order kinetics with a t/2 of -2 h. Similar disappearance kinetics were observed for two subjects presenting in the emergency room with immediate type reactions, one with severe asthma after indomethacin ingestion, the other with systemic anaphylaxis after a bee sting. Histamine levels declined rapidly and were back to baseline by 15-60 min. Measured levels of tryptase in serum or plasma were not diminished by up to four freeze-thaw cycles. Incubation of serum samples taken from subjects with elevated levels of tryptase at 22 and 370C indicated that > 50% of endogenous tryptase was still detected after 4 d. Purified tryptase added to serum or plasma and incubated as above was less stable: -50% of exogenous tryptase in serum and -15% in plasma was detected after 2 d of incubation. Therefore, optimally samples should be stored frozen, but even those stored at room temperature for up to 4 d should be satisfactory. The best time to obtain samples for tryptase determinations is 1-2 h after the precipitating event, but depending on the magnitude of the initial response elevated levels of tryptase may be present in the circulation for several hours.