Macromolecular absorption and cows' milk allergy

Article Abstract:

Antigenic macromolecules are large molecules that can activate an immune response. These substances are capable of moving through the mucosal membranes of the small intestine in amounts that may have immunological significance. The movement of antigenic macromolecules across intestinal mucosal membranes is increased in infants, and may contribute to the development of tolerance to certain elements in food products that cause an immune reaction (food antigens). Studies have suggested that patients with food allergies also have increased intestinal absorption of macromolecules, which may contribute to the allergic condition. Intestinal permeability can be assessed by measuring marker proteins in the blood or urine. Human alpha-lactalbumin is the dominant whey protein in human milk, and can be used as a marker of macromolecular absorption. The absorption of human alpha-lactalbumin was assessed in 28 children with suspected cows' milk allergy before the introduction of a diet free of cows' milk. Blood levels of alpha-lactalbumin were elevated, and gastrointestinal symptoms were present in 19 children and skin symptoms in nine. A total of 76 children who were placed on a diet free of cows' milk were then subjected to a cows' milk challenge. Twenty-six children developed symptoms and had higher alpha-lactalbumin levels than the 50 children without symptoms. The level of immune protein immunoglobulin E, which is increased in persons with allergy, did not correlate with blood alpha-lactalbumin levels in the allergic children. It is concluded that elevated levels of alpha-lactalbumin, indicating increased protein absorption, are characteristic of children with a cows' milk allergy. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Testing, Physiological aspects, Macromolecules, Intestinal absorption, Milk, Milk proteins, Food allergy in children, Pediatric food hypersensitivity

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Treatment of persistent pulmonary hypertension of the newborn: update

Article Abstract:

Some newborns have hypertension in pulmonary (lung) blood vessels, a state which is appropriate during fetal development but which, in newborns, causes inappropriate blood flow, hypoxemia (low blood oxygen levels), and acidosis (increased levels of acidic metabolites in blood) which can then cause further pulmonary vasoconstriction (blood vessel narrowing). Half of the pulmonary arteries in newborns contain muscles, and many of the stresses encountered during pulmonary hypertension can cause growth and development of these muscle cells, which then further decreases pulmonary vessel volume. Asphyxia, pneumonia, or infection are among the other disorders which may cause pulmonary hypertension in newborns. The death rate in affected infants may be as high as 60 percent. Because there are multiple causes of this disorder, no single treatment is appropriate. Both the underlying cause and the hypertension need treatment. This includes antibiotic therapy, maintenance of blood pressure with drugs and fluids, treatment with alkali to counteract acidosis, and management of lung function with ventilation and possibly oxygenation and muscle relaxants. No drugs which can dilate only pulmonary blood vessels are available. Thus, systemic vasodilators have been used, including modulators of synthesis of prostaglandins and related hormones, calcium channel blockers, and magnesium, which may be very effective. Studies of each of these drugs in pulmonary hypertension are reviewed. Further research on the effects of these therapeutic options is needed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Persistent fetal circulation syndrome, Pulmonary hypertension

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