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Relationships between symptoms and changes in breast physiology during lactation mastitis

Fetherston, C.M., Lai, C.T. and Hartmann, P.E. (2006) Relationships between symptoms and changes in breast physiology during lactation mastitis. Breastfeeding Medicine, 1 (3). pp. 136-145.

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    Link to Published Version: http://dx.doi.org/10.1089/bfm.2006.1.136
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    Abstract

    OBJECTIVE: The objective was to investigate changes in milk composition that reflect variations in breast permeability, milk synthesis, and immune response in women before, during, and after mastitis. METHODS: Mothers (n = 26) were followed prospectively from day 5 postpartum to the end of their lactation. Milk from each breast, blood, 24-hour urine samples, and data on breast and systemic pathologies were collected at reference intervals during the first 3 months postpartum, daily during the occurrence of any breast inflammation, and 7 days after resolution of symptoms, and was analyzed using mixed-model analysis (repeated measures). RESULTS: There was a significant difference in sodium (p < 0.001), chloride (p < 0.001), serum albumin (p < 0.02) and lactose (p < 0.003) in the breast with mastitis when compared with both the contralateral asymptomatic breast and "healthy" breasts. Inflammation of the whole breast was a significant predictor for a decreased glucose (p < 0.01) and hyperacute systemic symptoms predicted a decrease in milk glucose (p < 0.03) and an increased lactoferrin (p < 0.05) and sIgA (p < 0.03). CONCLUSIONS: There is an increased breast permeability, reduced milk synthesis, and increased concentration of the immune components sIgA and lactoferrin with increasing severity of breast and systemic symptoms. The changes observed in milk composition during periods of increased breast permeability cannot be solely explained by the current theory of permeability of the paracellular pathway and further research in this area is required.

    Publication Type: Journal Article
    Publisher: Mary Ann Liebert Inc.
    Copyright: © Mary Ann Liebert, Inc.
    URI: http://researchrepository.murdoch.edu.au/id/eprint/6691
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