The accumulation of neutrophils in the skin lesions, similar with Sweet syndrome (acute febrile neutrophilic dermatosis) supporting the inclusion of PG within the spectrum of neutrophilic dermatoses [3]. The frequency of pathergy (development of new lesions or aggravation of existing ones following local injuries) suggests altered inflammatory responses to nonspecific stimuli. The widely accepted hypothesis is that PG has a complex and multifactorial pathogenesis, including genetic predisposition, paraneoplastic check details or para-immune phenomena, and undefined infectious agents [4, 5]. The most common clinical classification includes

four major types: ulcerative, pustular, bullous, and vegetative [6, 7]. Other particular forms have also been described: peristomal, genital, mucosal, extracutaneous, and postoperative [8–11]. Herein, the authors present a patient with postoperative PG in association with renal cell carcinoma and chronic lymphocytic leukemia. Case Report A 62-year-old male patient presented with renal carcinoma. The tumor was removed by partial nephrectomy in cold ischemia without undesirable events. Histology confirmed a well-differentiated

renal cell carcinoma with histologically negative margins. The patient also suffered from stable chronic lymphocytic leukemia treated with rituximab and hypothyroidism under substitution with l-thyroxine. Five days after nephrectomy, a progressive painful

ulceration developed rapidly at the site of incision. Selleckchem S3I-201 The lesion was deep and had an overhanging violaceous border. The left lumbar area was indurated and erythematous (Fig. 1a). Fig. 1 Pyoderma gangrenosum: a extensive ulceration at the site of incision with violaceous borders at the periphery; b the ulceration after 12 days of corticotherapy The patient aminophylline became febrile and his white blood cells (WBC) rose from 6,100 to 56,000/mm3. C-reactive protein (CRP) levels increased from 1.4 to 259 mg/L. At this point, a wound selleck kinase inhibitor infection was suspected. He was empirically treated with antibiotics (ciprofloxacin, then imipenem and doxycycline) but its condition progressed relentlessly. Ultrasound and computer tomography scans failed to identify an abscess. Surgical wound revision did not identify any sign of bacterial infection. Preoperative, intraoperative, and postoperative wound culture remained negative. However, blood culture was positive for Staphylococcus haemolyticus, and imipenem was changed for vancomycin. Despite broad-spectrum antibiotics, there was a sustained expansion of the skin lesion. PG was suspected and the patient was referred to a dermatologist. A biopsy specimen of the edge of the ulceration showed a phlegmonous nonspecific inflammation without being able to differentiate between a necrotizing wound infection and PG. Microbiology of the skin specimen was negative.