The authors have indicated no significant interest with commercial supporters.I ntractable wounds are caused by extrinsic factors 1 (e.g., burns, trauma, pressure sores, radiation ulcers, contact dermatitis); arterial insufficiency secondary to arteriosclerosis obliterans, 2 Buerger's disease (thromboangiitis obliterans), collagen diseases, 3 vasculitis, diabetes mellitus, 4 and calciphylaxis or calcific uremic arteriolopathy; 5 venous insufficiency secondary to stasis dermatitis, varicose veins, and deep venous thrombosis; neural factors (spina bifida, diabetes mellitus); severe infections (aerobic and anaerobic bacteria, fungi, acid-fast bacilli, virus 6 ); malignancies (amelanotic melanoma, squamous cell carcinoma, basal cell carcinoma, angiosarcoma, B cell lymphoma, epithelioid sarcoma); and other conditions related to diseases peculiar to dermatology, including pyoderma gangrenosum and bullous diseases. Although most intractable wounds are relatively easy to diagnose macroscopically, the combination of those risk factors may mask important factors underlying the true nature of the disease. We recently experienced a case of intractable ulcers that showed different clinical courses between the medial ( Figure 1) and lateral ( Figure 2) sites on the left lower leg of a patient with diabetes mellitus. The medial ulcers were caused by pyoderma gangrenosum and a methicillin-resistant Staphylococcus aureus (MRSA) infection, whereas in addition to those two factors, arterial insufficiency secondary to an arteriovenous fistula and steroidinduced diabetes mellitus caused the lateral ulcers. The ischemic characteristics were totally masked because of the irregular, boggy, blue-red ulcers with undermined borders surrounding a purulent necrotic base, characteristic of pyoderma gangrenosum.
Case ReportA 62-year-old man with a past history of bad teeth, hemorrhoids, and cigarette smoking for 43 years had pyoderma gangrenosum treated with 5 mg/day (d) of prednisolone and 75 mg/d of diaminodiphenylsulphone for 12 years on his left lower leg and steroidinduced diabetes mellitus treated with insulin for 10 years. The patient was admitted to our hospital on February 8, 2006, because the chronic, painful wounds with irregular borders on his left lower leg were refractory to local wound care, and prednisolone had been increased to 20 mg/d since October 18, 2005. The clinical appearances of the medial ( Figure 1A) and lateral (Figure 2A) wound sites of his leg were similar, with no edematous swelling on admission.The results of laboratory examination revealed a white blood cell count of 9.6 Â 10 3 /mL; C-reactive protein of 12 mg/L; erythrocyte sedimentation rate of 22 mm/hour; fasting plasma glucose of 280 mg/dL; hemoglobin A1c 7.6%; platelet factor 4 of 27 ng/mL; X-thromboglobulin of 76 ng/mL; soluble interleukin-2 receptor of 511 U/mL; high neutrophil migration in response to classic chemoattractants, indicating the inflammation, uncontrolled diabetes mellitus, and activation of platelets and neutrophil activities. The patient ...