Full Text: THE NEW ENGLAND JOURNAL OF MEDICINE

Vol 348, March 13, 2003

* Factors associated with the development of peanut allergy in childhood. G. Lack, D. Fox, K. Northstone, et al, for the Avon Longitudinal Study of Parents and Children Study Team. 977-985.

* Effect of anti-lgE therapy in patients with peanut allergy. D.Y.M. Leung, H.A. Sampson, J.W. Yunginger, et al, for the TNX-901 Peanut Allergy Study Group. 986-993.

Vol 348, March 20, 2003

[] Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. I.S. Farooqi, J.M. Keogh, G.S.H. Yep, E.J. Lank, T. Cheetham, and S. O'Rahilly. 1085-1095.

* Binge eating as a major phenotype of melanocortin 4 receptor gene mutations. R. Branson, N. Potoczna, J.G. Kral, K.-U. Lentes, M.R. Hoehe, and F.F. Horber. 1096-1103.

Vol 348, April 24, 2003

* Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. E.E. Calle, C, Rodriguez, K. Walker-Thurmond, and M.J. Thun. 1625-1638.

Factors associated with development of peanut allergy in childhood Sensitization to peanut protein may occur in children thrbugh contact of peanut oil with inflamed skin. The association between peanut allergy and soy protein intake could arise from cross-sensitization through common epitopes. Confirmation of these risk factors in future studies could lead to new strategies to prevent sensitization in infants who are at risk for subsequent peanut allergy. Data were obtained from the Avon Longitudinal Study of Parents and Children, a geographically defined cohort study of 13,971 preschool children. Data were collected prospectively on the whole cohort, and detailed information was collected retrospectively by interviewing parents of children with peanut reactions and children in 2 control groups. Control subjects were 140 healthy children randomly selected from the cohort (n= 140) and 70 children whose mothers had a history of eczema and who had had eczema themselves in the first 6 months of life. Forty-nine children had a convincing history of peanut allergy; peanut allergy was confirmed using double-blind peanut challenge in 23 of 36 children tested. There was no evidence of prenatal sensitization from the maternal diet, and peanut-specific immunoglobulin E was not detectable in cord blood. Peanut allergy was independently associated with intake of soy milk or soy formula (odds ratio [OR] = 2.6), rash over joints and skin creases (OR = 2.6), and oozing or crusted rash (OR = 5.2). Analysis of interview data showed a significant independent relationship between peanut allergy and use of skin preparations containing peanut oil (OR = 6.8).

Effect of anti-IgE therapy in patients with peanut therapy TNX-901 is a humanized immunoglobulin G1 (IgG1) monoclonal antibody against IgE that recognizes and masks an epitope in the CH3 region of IGE responsible for binding to the high-affinity Fc [member of] receptor on mast cells and basophils. This study found that a 450-rog dose of TNX-901 significantly and substantially increased the threshold of sensitivity to peanut on oral food challenge from a level equal to about half a peanut (178 mg) to almost 9 peanuts (2,805 mg), an effect that should provide protection against most situations in which peanuts are accidentally ingested. Hypersensitivity to peanut was confirmed and the threshold dose of encapsulated peanut flour was established using a double-blind, placebo-controlled oral food challenge in 84

patients with a history of immediate hypersensitivity to peanut. Subjects were randomly assigned to receive 4 doses of 150, 300, or 450 mg TNX-901 or placebo subcutaneously at 4-week intervals. Patients underwent a final oral food challenge within 2 to 4 weeks after the fourth dose. From group mean baseline thresholds of sensitivity of 178 to 436 mg peanut flour, mean increases in the oral-food-challenge threshold were 710, 913, 1,650, and 2,627 mg in the groups that received placebo and 150, 300, and 450 lug TNX-901, respectively; the increase in groups that received the study drug vs placebo was significant only in those who received the 450-mg dose. TNX-901 was well tolerated.

Binge eating as a phenotype of melanocortin 4 receptor gene mutations Binge eating is a major phenotypic characteristic of subjects with a mutation in the melanocortin 4 receptor (MC4R) gene, a candidate gene for control of eating behavior. The authors sequenced the complete MC4R coding region, the region of the proopiomelanocortin gene (POMC) encoding the a melanocyte-stimulating hormone, and the leptin-binding domain of the leptin receptor (LEPR) gene in 469 severely obese white adults (370 women and 99 men, mean age = 41.0 [+ or -] 0.5 years, mean body mass index [BMI] = 44.1 [+ or -] 2.0). Fifteen women and 10 men without a history of dieting or a family history of obesity served as normal-weight control subjects (mean age = 47.7 [+ or -] 2.0 years, mean BMI = 21.6 [+ or -] 0.4). The authors collected detailed phenotypic data, including information on body composition, resting energy expenditure, diet-induced thermogenesis, serum leptin level, and eating behavior. Twentyfour obese subjects (5.1%) and one control subject (4.0%) had MC4R mutations, including 5 novel variants. Twenty of the 24 obese subjects with an MC4R mutation were matched for age, sex, and BMI with 120 of the 445 obese subjects without an MC4R mutation. All mutation carriers reported binge eating, as compared with 14.2% of subjects without mutation; this difference was significant. The prevalence of binge eating was similar among carriers vs noncarriers of mutations in the leptinbinding domain of LEPR. No mutations were found in the region of POMC encoding a melanocyte-stimulating hormone.

Overweight, obesity, and mortality from cancer Body weight appears to be positively related to death rate for all cancers combined and for cancers at several specific sites. Subjects were 404,576 men and 495,477 women (aged [greater than or equal to] 30 years) who participated in the Cancer Prevention Study II and were free of cancer at enrollment in 1982. Each subject's body mass index (BMI) was calculated from their self-reported height and weight at baseline; subjects who had lost [greater than or equal to] 10 lbs during the previous year were excluded. During 16 years of follow-up, 57,145 subjects died from cancer. Among subjects with BMI [greater than or equal to] 40.0 vs 18.5 to 24.9, the relative risk of death from all cancers combined was 1.52 in men and 1.62 in women. In both men and women, BMI was significantly associated with relative risk of death due to non-Hodgkin's lymphoma; multiple myeloma; and cancer of the esophagus, colon and rectum, liver, gallbladder, pancreas, and kidney. BMI was also significantly positively associated with relative risk of death due to cancer of the stomach and prostate in men and cancer of the breast, uterus, cervix, and ovary in women. Data from this study suggest that current patterns of overweight and obesity in the U.S. population could account for 14% of all deaths from cancer in men and 20% of those in .women.

Source Citation   (MLA 7th Edition) 

"The New England Journal of Medicine." Journal of the American Dietetic Association 103.8 (2003):

1084+. Gale Light Arts, Economy, Education, Humanities & Social Science. Web. 9 Dec. 2014.

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