Sweat gland atrophy of the heel in diabetic patients with angiopathy.

As diabetic foot ulcer (DFU) severely affects prognosis and quality of life of patients with DM, it is an urgent issue to establish effective preventive and treatment methods for DFU. One known mechanism of DFUs is through the formation of fissures. Oe et al. have previously identified angiopathy as a risk factor for deep fissures (Oe et al. 2012), independent of autonomic neuropathy, which was previously known as another factor for fissures. In other words, treatment directly targeting angiopathy is also necessary to prevent fissures, in addition to the use of moisturising agents. As the mechanism of deep fissure formation because of angiopathy remains unclear, no definitive treatment strategy can yet be established. Fissures are often associated with decreased perspiration. Decreased perspiration of the upper arm while in tourniquet has been reported (Van Heyningen & Weiner 1952, Collins et al. 1959). This finding suggests a possible mechanism, in that impaired blood circulation causes decreased production of sweat from the sweat gland. Furthermore, long-term impaired blood circulation might cause the disuse atrophy of sweat glands. However, there have been no reports addressing which possibility is correct. In this study, a noninvasive modality, skin microscopy, was used to evaluate sweat gland atrophy of the heel, a common location for fissures. In localised scleroderma lesions, decreased perspiration and a decrease in number of sweat pores have been observed, and they have been reported to correlate with pathologic findings of sweat gland atrophy (Serup 1984). Thus, the number of sweat pores observed on microscopy was used as a surrogate index for sweat gland atrophy.