Pyoderma gangrenosum after surgery for forefoot deformity in a patient with rheumatoid arthritis: A case report.

Pyoderma gangrenosum (PG) is a rare inflammatory skin disease characterised by skin ulcers that are associated with autoimmune diseases. Although the effectiveness of immunosuppression with glucocorticoids and tumour necrosis factor inhibitors in treating PG has been reported, the utility of negative-pressure wound therapy (NPWT) for severe ulcerative lesions in patients with PG remains controversial. Herein, we report the case of a 76-year-old woman with rheumatoid arthritis who developed PG after undergoing surgery for a forefoot deformity. The patient showed improvement in deep ulcer lesions through NPWT while receiving treatment with abatacept and systemic glucocorticoids. Subsequent topical glucocorticoid therapy led to the remission of the PG. This case suggests that NPWT, when used under immunosuppressive conditions, does not exacerbate the pathergy and may be beneficial for treating severe ulcerative PG.

Olaparib-Induced Purpuric Drug Eruption in a Patient with Castration-Resistant Prostate Cancer.

Olaparib is recently approved as an anti-tumor agent for several cancers, including castration-resistant prostate cancer, which inhibits poly (adenosine diphosphate-ribose) polymerase, a DNA repair factor. Since olaparib is a newly approved drug, there are few reports of skin disorders that may be triggered by olaparib administration. In this report, we present a case with an olaparib-induced drug eruption presenting multiple purpuras on the patient's fingers and fingertips. The present case suggests that olaparib might induce purpura as nonallergic drug eruption.

Effect of ketoconazole on the pharmacokinetics of the dipeptidyl peptidase-4 inhibitor teneligliptin: an open-label study in healthy white subjects in Germany.

OBJECTIVE: The aim of this study was to examine the effect of ketoconazole, a potent cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp) inhibitor, on teneligliptin pharmacokinetics and to evaluate the safety of combined administration of teneligliptin with ketoconazole. METHODS: This open-label, fixed-sequence study was conducted in 16 healthy adult volunteers in Germany. On day 1, under fasting conditions, 20 mg of teneligliptin was administered to evaluate the pharmacokinetics of teneligliptin alone. For 3 days (days 8-10), 400 mg of ketoconazole was administered once daily. On day 11, teneligliptin 20 mg and ketoconazole 400 mg were concurrently administered, and for 2 days (days 12 and 13), ketoconazole was administered once daily. The pharmacokinetic parameters (Cmax, Tmax, AUC, terminal t½, apparent total plasma clearance, and Vd during the terminal phase) of teneligliptin on days 1 and 11 were calculated. The safety profile was evaluated based on adverse events and clinical findings. To investigate the role of human P-gp in membrane permeation of teneligliptin, an in vitro study was performed to measure the transcellular transport of teneligliptin across monolayers of human P-gp-expressing cells and control cells. RESULTS: For Cmax and AUC, the geometric least squares mean ratios (90% CIs) of teneligliptin with ketoconazole to teneligliptin alone were 1.37 (1.25-1.50) and 1.49 (1.39-1.60), respectively. There was no change in t½ of the terminal elimination phase. In addition, the tolerability of teneligliptin coadministered with ketoconazole was acceptable. The in vitro study revealed corrected efflux ratios for teneligliptin of 6.81 and 5.27 at teneligliptin concentrations of 1 and 10 µM, respectively. CONCLUSIONS: Because the exposure to teneligliptin in combined administration with ketoconazole, a potent CYP3A4 and P-gp inhibitor, was less than twice that of administration of teneligliptin alone, it is suggested that combined administration of teneligliptin with drugs and foods that inhibit CYP3A4 should not cause a marked increase in exposure. The results of our in vitro study suggest that teneligliptin is a substrate of P-gp. CLINICAL TRIAL REGISTRATION: EudraCT No. 2009-016652-51.