ABSTRACT
BACKGROUND: Peristomal pyoderma gangrenosum (PPG) presents multiple challenges for healthcare providers. The diagnosis of PPG may be delayed, and it may be mistaken for an irritant dermatitis or an infection. Patients with ostomies secondary to inflammatory bowel disease (IBD) may experience PPG. Issues related to PPG include difficulty maintaining a seal of the ostomy pouching system and preventing contamination of the painful, necrotic ulcerations characteristic of this condition. Treatment focuses on the appropriate assessment of the ulcers, successful pouch application, and proper management of IBD through a collaborative effort of both dermatologists and certified WOC nurses (CWOCN). CASES: We treated 3 patients diagnosed with Crohn's disease (CD) who developed refractory PPG. All 3 were treated with a topical steroid lotion, prednisone, and adalimumab or a combination of these agents. Ostomy products and application were tailored to prevent leakage and protect areas of ulceration. All ulcers were healed within 6 months of our initial consultation. CONCLUSION: We successfully managed 3 patients with CD and PPG with appropriate ostomy care, including revision of the ostomy pouching techniques, topical steroid treatment, and treatment based on assessment of ulcer status by the dermatologist and the WOC nurse.
Subject(s)
Adalimumab/therapeutic use , Anti-Inflammatory Agents/therapeutic use , Glucocorticoids/therapeutic use , Inflammatory Bowel Diseases/complications , Ostomy/adverse effects , Pyoderma Gangrenosum/drug therapy , Steroids/therapeutic use , Surgical Stomas/adverse effects , Adalimumab/administration & dosage , Administration, Topical , Adult , Aged, 80 and over , Anti-Inflammatory Agents/administration & dosage , Crohn Disease/diagnosis , Crohn Disease/therapy , Female , Glucocorticoids/administration & dosage , Humans , Postoperative Complications , Prednisone/administration & dosage , Prednisone/therapeutic use , Pyoderma Gangrenosum/diagnosis , Steroids/administration & dosage , Treatment OutcomeSubject(s)
Carbonic Anhydrase Inhibitors/adverse effects , Dermatitis, Allergic Contact/etiology , Eyelids , Facial Dermatoses/chemically induced , Ocular Hypertension/drug therapy , Sulfonamides/adverse effects , Thiophenes/adverse effects , Administration, Cutaneous , Adrenal Cortex Hormones/therapeutic use , Aged, 80 and over , Carbonic Anhydrase Inhibitors/administration & dosage , Dermatitis, Allergic Contact/drug therapy , Facial Dermatoses/drug therapy , Female , Humans , Ophthalmic Solutions , Sulfonamides/administration & dosage , Thiophenes/administration & dosageSubject(s)
Antibodies, Monoclonal, Humanized/administration & dosage , Arthritis, Psoriatic/diagnosis , Arthritis, Psoriatic/drug therapy , Dermatitis, Atopic/chemically induced , Dermatitis, Atopic/pathology , Infliximab/adverse effects , Biopsy, Needle , Dermatitis, Atopic/drug therapy , Disease Progression , Dose-Response Relationship, Drug , Drug Administration Schedule , Humans , Immunohistochemistry , Infliximab/therapeutic use , Japan , Male , Middle Aged , Prognosis , Psoriasis/diagnosis , Psoriasis/drug therapy , Risk Assessment , Severity of Illness Index , Treatment OutcomeABSTRACT
Numerous reports have shown that psoriasis is associated with obesity and leptin. However, few reports are available on the association between serum leptin levels and leptin gene expression in SAT of psoriasis patients. To clarify this point, we examined serum leptin levels and expression levels of leptin messenger RNA (mRNA) in subcutaneous adipose tissue (SAT) of psoriasis patients. 17 psoriasis vulgaris patients and 6 non-obese control patients who underwent skin surgery were enrolled in this study. We measured serum leptin levels. SAT samples in psoriasis patients were taken from beneath the lesional psoriatic skin at the time of skin biopsy. Leptin mRNA expression in SAT was measured using quantitative real-time reverse transcription polymerase chain reaction (real-time RT-PCR) amplification. Leptin mRNA expression showed a positive correlation with serum leptin levels and BMI. We classified psoriasis patients into two groups according to BMI: the group of non-obese psoriasis patients (BMI < 25, n = 7), and the group of obese psoriasis patients (BMI ≥ 25, n = 10). PASI score, serum leptin levels and Leptin mRNA expression in SAT were significantly higher in the obese psoriasis patients than in the non-obese psoriasis patients. Leptin mRNA expression in SAT was correlated with circulating levels of leptin, the severity of psoriasis, and obesity in psoriasis patients. Serum leptin levels and leptin mRNA expression levels in SAT of non-obese psoriasis patients were not significantly different from those of non-obese controls. The altered secretion of leptin by SAT may be related to the severity of psoriasis.
