The authors report their experience with 23 sites of hidradenitis suppurativa, including cases with musculocutaneous flap repair, and discuss the surgical methods applied. Twenty-three sites in 19 patients with chronic inflammatory skin lesions were reviewed. The lesions were divided into two groups: The limited group was comprised of mild lesions, which appear isolated and have limited abscesses without sinus tract formations. The severe group was compromised of severe lesions, which included diffuse, multiple abscesses with severe sinus tract formation and fibrosis. Nine sites were limited and 14 sites were severe. After resecting the lesion, the defect was covered with a split-thickness skin graft (four sites were limited, nine sites severe), a musculocutaneous flap (five sites severe), primary closure (four sites limited), and a local skin flap (one site limited). In six sites in 6 severe-group patients, local recurrence occurred. The local recurrence rate differed significantly between the limited and the severe groups. The reason for this may be because the lesions in the limited group could be resected completely, whereas the lesions in the severe group were diffuse and total resection was sometimes difficult for various reasons. The method of surgical repair did not affect the local recurrence rate. In recurrent cases, four sites treated with skin grafting required further surgical treatment, and two sites treated with musculocutaneous flaps were controlled with oral antibiotics. In conclusion, sufficient resection of the lesion is the most important issue in treating follicular occlusion triad disease. In lesions that can be resected completely, the surgical procedure to cover the lesions should be selected to suit the size and site of the defect. However, in cases that cannot be resected completely, a musculocutaneous flap is recommended instead of a skin graft for enhanced postoperative management of the recurring wound, and its contribution to aesthetic and functional improvement.

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The authors investigated the expression of p53, p21(WAF-1), Bax protein, and apoptosis to elucidate the cellular response to ischemia-reperfusion of skeletal muscle using the rat lower limb model. The rat left lower limb was dissected in the inguinal region, isolating the bony femoral muscles, and the femoral vessels were clamped to produce an ischemic condition. After 3 or 6 hours, the clamps were removed and the gastrocnemius muscle was resected at various times up to 72 hours after reperfusion. Five specimens of the muscle were obtained at each time point from 5 rats. When any rat died during the study, additional rats were used until 5 specimens could be obtained from 5 rats at each time point. The expression of three proteins was detected by Western blot analysis. The apoptotic cells were detected using terminal deoxytransferase-mediated dUDP (deoxyuridine[-5']diphosphate) nick-end labeling assay. Histopathological study showed severe interstitial edema and leukocyte infiltration at 6 hours of ischemia compared with 3 hours of ischemia. Moreover, at 6 hours of ischemia, muscle fiber fragmentation was observed at 72 hours after reperfusion whereas no fragmentation was found at 3 hours of ischemia. At 3 hours of ischemia, p53 and p21(WAF-1) accumulated after reperfusion, and there was a time lag in the time of onset of elevation and the peak time point between these two proteins. The level of Bax protein did not elevate and the rate of apoptotic cells did not increase. At 6 hours of ischemia, p53 and p21(WAF-1) also accumulated, but the kinetics of p21(WAF-1) were similar to that of p53 in the time of onset of elevation and the peak time point after reperfusion. In addition, the level of Bax protein increased and apoptosis was induced. These results demonstrated that p53 and p21(WAF-1) accumulated after 3 and 6 hours of ischemia of skeletal muscle during reperfusion. Moreover, it was demonstrated that the kinetics of induced p53, p21(WAF-1) and Bax protein differ between 3 hours and 6 hours of ischemia, and it is speculated that this difference plays an important role in determining the consequence of the cell exposed to ischemia.