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BACKGROUND: Necrotizing fasciitis is a severe bacterial skin infection that spreads quickly and is characterized by extensive necrosis of the deep and superficial fascia resulting in the devascularization and necrosis of associated tissues. Because of high morbidity and mortality, accurate diagnosis and early treatment with adequate antibiotics and surgical intervention are vital. And timely identification and treatment of complications are necessary to improve survival of patient. CASE SUMMARY: We report a case of necrotizing fasciitis caused by Staphylococcus aureus in a patient using high doses of glucocorticoid and suffering from secondary diabetes mellitus. He was admitted to our hospital due to redness and oedema of the lower limbs. After admission, necrotizing fasciitis caused by Staphylococcus aureus was considered, and he was discharged after B-ultrasound drainage and multiple surgical operations. In the process of treatment, multiple organ functions were damaged, but with the help of multi-disciplinary treatment, the patient got better finally. CONCLUSION: The key to successful management of necrotizing fasciitis is an early and accurate diagnosis. The method of using vacuum sealing drainage in postoperative patients can keep the wound dry and clean, reduce infection rate, and promote wound healing. Interdisciplinary collaboration is a vital prerequisite for successful treatment.
RESUMEN
Adipokine adiponectin (APN) has been recently reported to play a role in regulating bone mineral density (BMD). To explore the mechanism by which APN affects BMD, we investigated BMD and biomechanical strength properties of the femur and vertebra in sham-operated (Sham) and ovariectomized (OVX) APN knockout (KO) mice as compared to their operated wild-type (WT) littermates. The results show that APN deficiency has no effect on BMD but induces increased ALP activity and osteoclast cell number. While OVX indeed leads to significant bone loss in both femora and vertebras of WT mice with comparable osteogenic activity and a significant increase in osteoclast cell number when compared to that of sham control. However, no differences in BMD, ALP activity and osteoclast cell number were found between Sham and OVX mice deficient for APN. Further studies using bone marrow derived mesenchymal stem cells (MSCs) demonstrate an enhanced osteogenic differentiation and extracellular matrix calcification in APN KO mice. The possible mechanism for APN deletion induced acceleration of osteogenesis could involve increased proliferation of MSCs and higher expression of Runx2 and Osterix genes. These findings indicate that APN deficiency can protect against OVX-induced osteoporosis in mice, suggesting a potential role of APN in regulating the balance of bone formation and bone resorption, especially in the development of post-menopausal osteoporosis.