SummaryThe present data suggest that perinatal asphyxia may result in a transfer of blood, in utero, from placenta to fetus. The data contain no suggestion that asphyxia causes pooling of fetal blood in the placenta.
\s=b\Bronchial asthma in childhood is a major pediatric problem for the physician, both as an acute emergency and as a chronic disease. To adequately manage asthma, one must have a firm understanding of its pathogenesis, and the clinical aspects of diagnosis and therapy. We review important developments in the area of the basic mechanisms causing bronchial obstruction, and methods of measuring the abnormalities present. This presentation includes the fields of neuropharmacology, biochemistry, immunology, and pulmonary physiology. With this background, the clinical aspects of diagnosis and therapy are explored. The role of the allergy history, skin testing, measurement of serum IgE antibodies, and target organ provocation testing are placed in perspective. Therapy involving avoidance measures, use of pharmacologic agents and injection therapy with inhalant allergens are discussed in detail.(Am J Dis Child 130: [890][891][892][893][894][895][896][897][898][899] 1976) Many new and exciting advances in the understanding of bron¬ chial asthma have been made in the last decade. These developments have resulted in a more rational approach to the asthmatic child. The review presented here summarizes this new information by considering the basic scientific aspects of the pathogenesis of asthma, followed by discussion of the recent developments in diagnosis and therapy. PATHOGENESIS OF BRONCHIAL ASTHMA NeuropharmacologyBronchial asthma can no longer be viewed solely as an immunologie disease. The clinical observation that several stimuli, including chemical mediators, irritants, certain respira¬ tory infections, emotional and physi¬ cal factors, as well as allergen chal¬ lenge, can result in bronchospasm, created the need for a broader concept in underlying abnormality.In the early 1960s, Szentivanyi1 advanced the theory of /3-adrenergic blockade as a possible unifying path¬ ogenic mechanism in asthma. This theory proposes that many of the stimuli that result in the clinical syndrome of asthma do so by causing release of potent chemical mediators of inflammation such as the kinins, slow-reacting substance of anaphy¬ laxis (SRS-A), histamine, serotonin, and acetylcholine. The mediators, in turn, cause both bronchoconstriction and secretion of epinephrine as a homeostatic response. If /5-adrenergic receptors are normally responsive, activation by epinephrine will balance concurrent a-adrenergic and cholinergic receptor stimulation, and airway patency will be maintained. However, if /3-receptors are defective, bronchoconstriction will result.Evidence for generalized /^-blockade in asthma includes metabolic, pulmo¬ nary, and hématologie changes. There is less elevation of serum glucose, lactate, and pyruvate levels following administration of the ß-adrenergic stimulants, isoproterenol hydrochloride and epinephrine hydrochloride, in asthmatics than in normal subjects.2 ;' Administration of the /5-blocking agent, propranolol hydrochloride, leads to increased airway resistance in asthmatic patients'; in patients with allergic ...
Ihrinn a measles immunjzation camoai~n hlood sam?les were collected from 203 children before vaccination. Follow un specimens were collected from 125 children 3 ~rlcs. later and from 98 chtldren 10 mos. later. Of the 125 children with follow up study, 88 had been previously vnccinated. 10 had a I~istory of measles and 27 denied vacctnntion or illness. !kanles llAT antibody geometric nesn titers (C!ms) were 13. (day 01, 33 (3 wks.), and 23 (111 mos.). Twenty-six of the 125 llsd !!.\I titers of -5 prior to vaccination and sho!red a 24-fold antitiodv titer rise. Ig:: measles ontibodv was detected in 12 of these children after protein-A and 2-!E treatmentSwith a C'PT at 3 weeks and 10 months of El and 40 respectively. There was no history of measles exposure or vaccination in this group. Tn the remaining 14 children vith initial ttters < 5 no Kx!! antibody response was detected. and despite n &-fold increase in IlAI titer at 3 wks. (C'IT 28). the 10 aonth titer had dropped considerably (C\V 9). Ten of these 14 children had a history of previous measles vaccination. The remaining 99 children had detectable initial titers between 5 and 320. After grouping these according to their pre-booster titers, no significant cllange in Q R s was ol~served when dsv 0. 3 wk. and 10 mo. results were compared. Our study suggests that IIAT antihodv titers in children previously imnunologically stimulated against measlen are not altered significantly bv revaccination, even when the prebooster titers are low or not detectable. Monocytea from two unrelated C3 deficient patients, one of whom has keen described (J. Clin. Invest. 56, 703, 1975). were examined in culture. Serum from each of the patients contained less than It of the normal C3 concentration (not due to hypercatabolim) but monocytes from each produced C3 at approximately 25% of the nonnal rate when studied after two weeks ~JL yLtyp. The C3 produced in vitro by monocytes from one of the patients was shown to have thy m i i o ular weight of normal serum C3 and to dissociate appropriately under reducing conditions. Monocytes from C3 deficient patients could not be distinguished from normals on the basis of morphology, roaetting with C3 coated erythrocytes, or rates of C2 and total protein synthesis. The ability of monocytes from C3 deficient patients to produce C3 in vitro is in contrast to studies of monocytes from C2 deficient humans and macrophages from C4 deficient guinea pigs in which specific biosynthetic defects for C2 and C4, respectively, persisted in vitro. Monocyte chemotactic defects have previously been described in several conditions. We have noted marked defects (>2 S.D.) in one patient with chronic mucocutaneoua candidiasis and 4/29 atients with atopic dermatitis. In 8 patients on salicylate tRerspy, a mean decrease of monocyte chemotaxis of 25% was seen with salicylate levels >15 mgsX compared to a mean increase of 8% when neutrophil chemotaxia was concurrently measured. We also noted decreased monocyte chemotaxis in several seemingly normal subjects with absen...
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