A.R. Shipman; G.W.M. Millington

Disclosures

The British Journal of Dermatology. 2011;165(4):743-750. 

In This Article

Cutaneous Pathophysiology in the Obese

Obesity alters the epidermal barrier of the skin in some way, so that obese individuals have increased transepidermal water loss and dry skin.[16] Erythema is more pronounced, compared with controls,[17] and there is reduced microvascular reactivity.[18] The obese have larger skin folds and will sweat more profusely when overheated than the nonobese.[7] Obesity inhibits lymphatic flow[7] and alters collagen formation.[19] Delayed-type hypersensitivity is increased in obesity and reduces with weight reduction,[20] which may relate to an alteration in the balance of adipocyte cytokine production.[12,21]

The shape of the foot changes with obesity.[22] For example, obese children have a lower footprint angle and obese individuals have a wider forefoot width and also higher plantar pressures during standing and walking.[22] These pressure effects may eventually lead to plantar hyperkeratosis, a cutaneous sign of severe obesity.[22]

Interestingly, no differences have been found between the activity of sebaceous, apocrine or eccrine glands in the obese compared with the nonobese,[7] despite the evidence of changes in endocrine homeostasis with increasing weight gain (see also the section 'Adipocytokines, obesity and psoriasis').[2,5,6,10–13,23]

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