Yun Seok Jung

Diagnosing Acute Pyelonephritis with CT, 99mTc-DMSA SPECT, and Doppler Ultrasound: A Comparative Study

Purpose With growing interest in early imaging, the aim of our study was to define the most practical modality for routine clinical use for the diagnosis of acute pyelonephritis (APN). We compared the sensitivity of enhanced computerized tomography (CT), dimercaptosuccinic acid (DMSA) scintigraphy, and Doppler ultrasonography (DUS) by using clinical findings as the standard of reference. Materials and Methods A total of 207 APN patients (191 women, 16 men; mean age, 49.4 years; range, 17-88 years) were enrolled in this study. All the patients underwent imaging modalities during hospitalization. SPECT images were obtained 4 hours after injection of 99mTc-DMSA. Transverse and coronary CT images were obtained before and after injection of the contrast agent. DUS was performed in the longitudinal, transverse, and coronal planes. All the images were read independently by a single radiologist and a nuclear medicine specialist. The sensitivity of each modality for detecting APN was compared. Results CT showed significantly superior sensitivity compared with that of DUS (81.0% vs. 33.3%, respectively, n=147). DMSA scintigraphy also showed significantly superior sensitivity compared with that of DUS (74.7% vs. 33.3%, respectively, n=150). Compared with DMSA scintigraphy, CT showed superior sensitivity, but the difference was not statistically significant (81.0% vs. 74.8%, respectively, n=147, p=0.163). Conclusions For cases of clinically suspected APN, CT and DMSA scintigraphy appear to be equally sensitive and reliable for detecting APN, although CT is more practical in various fields. DUS was significantly less sensitive.

A hyaluronic acid-based microneedle patch to treat psoriatic plaques: A pilot open trial.

DEAR EDITOR, Psoriasis is a common, chronic, relapsing, inflammatory skin disease characterized by multiple erythematous papules and plaques with silvery scales. It affects 0 5–3% of the world’s population. Recently, great advances have been made in the treatment of psoriasis, including the introduction of targeted biological agents. However, topical treatment remains important; most patients have mild disease affecting < 2% of the body surface area. Unfortunately, topical treatment is oily and sticky, and it takes time to reach full therapeutic effect, which results in poor patient compliance and consequently low therapeutic efficacy. The microneedle patch is a new drug delivery method that can effectively improve transdermal drug delivery. In this present study, we assessed whether a novel hyaluronic acid (HA)-based microneedle patch enhanced the therapeutic effects of topical agents in psoriasis. Ten patients with psoriatic plaques resistant to topical calcipotriol–betamethasone ointment (Daivobet ; LEO Pharma, Ballerup, Denmark) therapy for at least 4 weeks were enrolled from 1 May to 31 July 2016. One or more resistant psoriatic plaques were selected, and microneedle patches were placed over the thickest areas of the plaques after application of topical calcipotriol–betamethasone ointment. The patches were applied once daily at night for 1 week and removed the following morning. The patches were 26 9 26-mm-sized HA-

Acneiform eruptions caused by various second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukaemia.

DEAR EDITOR, Tyrosine kinase inhibitors (TKIs) are a novel, well-tolerated and promising class of anticancer drugs, commonly used to treat chronic myeloid leukaemia (CML). Imatinib was the first commercially available TKI, approved for the treatment of CML and gastrointestinal stromal tumours. The development of polyclonal resistance to imatinib, due to point mutations in the bcr-abl kinase domain, yielded second-generation TKIs including dasatinib, radotinib and nilotinib. These second-generation TKIs have shown higher rates of early optimal responses and fewer side-effects than imatinib. These new agents are indeed less toxic, but their range of activity is still not directed at tumour cells only. As a result, their use is associated with various systemic adverse events that go beyond the scope of the present review, but cutaneous side-effects are the most commonly reported. Nevertheless, there have been only a few reports of cutaneous adverse events caused by TKIs in patients with CML. To the best of our knowledge, this is the first report directly focused on acneiform eruptions due to second-generation TKIs in patients with CML. Herein, we report 10 cases of acneiform eruptions with or without rosacea-like eruptions caused by various second-generation TKIs in patients with CML. We studied 10 patients with CML treated with second-generation TKIs who were seen between November 2013 and May 2015. Patients with CML seen at the haematology department who presented with acneiform eruptions or rosacea-like eruptions were referred to our dermatology clinic (Fig. 1). Second-generation TKIs used for treatment included radotinib (n = 4), dasatinib (n = 4) and nilotinib (n = 2). No other drug was suspected to initiate these eruptions. Patients were interviewed and examined by a single dermatologist, and all diagnoses were made clinically. The characteristics of the patients with CML with skin lesions, and their treatment outcomes are described in Table 1. The pathophysiology of cutaneous eruptions caused by TKIs is unclear. It has been reported that the TKI-induced rosacealike eruptions may be associated with a dermal matrix abnormality and T-cell suppression caused by TKIs. TKIs inhibit the tyrosine kinase activities of bcr-abl and plateletderived growth factor receptor, blocking collagen synthesis and dermal matrix formation. Loosened connective tissue support for cutaneous vessels may result in the recruitment of inflammatory mediators and metabolites, causing symptoms of rosacea such as telangiectasia, erythema, flushing and oedema. In addition, although we could not determine the factors that triggered the acneiform eruptions in our patients, it is suggested by recent studies that TKIs, like epidermal growth factor receptor (EGFR) inhibitors, induce alterations in follicular and epidermal cell homeostasis. However, in our experience there was a difference in the clinical presentation of acneiform eruptions depending on whether they were caused by TKIs or EGFR inhibitors. In EGFR inhibitor-induced acneiform eruptions, the lesions tend to be more follicular and the distribution of the lesions tends to be along the lateral borderline of the face and on the scalp, rather than on the face itself. In contrast, the lesions of TKI-induced acneiform eruptions are more consistent with the