Dermoscopy improves diagnostic accuracy for clinically amelanotic nodules.

BACKGROUND/OBJECTIVES: Amelanotic nodular melanomas are notoriously difficult to diagnose and are responsible for a disproportionate burden of melanoma mortality. It is important to distinguish them from other amelanotic nodules. This study aimed to describe the dermoscopic features of a series of nodular melanomas and other amelanotic nodules and to determine whether dermoscopy improves diagnostic accuracy. METHOD: Retrospective analysis of 150 clinically amelanotic nodules with macroscopic and dermoscopic images. RESULTS: In terms of classifying the nodules as malignant, dermoscopy was superior to unaided eye (specificity 89%; 95% CI 71-98% vs 67%; 95% CI 46-83%, P = 0.03). Dermoscopy enhanced sensitivity for the diagnosis of both amelanotic melanoma and SCC. In 19% of cases, using dermoscopy, the most likely diagnosis was changed from incorrect to correct. This included 26% of amelanotic melanomas which had a macroscopic misdiagnosis overturned to the correct diagnosis. Polymorphous vascular structures were more common in malignant nodules. 76% of amelanotic melanomas/Merkel cell carcinomas had polymorphous vessels compared with 38% of SCCs/KAs/BCCs and 22% of benign nodules (P < 0.001). CONCLUSION: Dermoscopy improves diagnostic accuracy for amelanotic melanomas and other amelanotic nodules. Although dermoscopy improves diagnostic accuracy for amelanotic melanomas, these aggressive melanomas remain diagnostically difficult.

Two cases of amoxycillin-induced follicular acute localised exanthematous pustulosis.

We report two cases of Caucasian women who developed folliculocentric pustulosis after exposure to amoxycillin. A literature review found that most amoxycillin-related pustular eruptions were reported as acute generalised exanthematous pustulosis (AGEP) or acute localised exanthematous pustulosis (ALEP). Histopathology from both our cases showed sterile suppurative folliculitis, which resolved on the cessation of amoxycillin.

Dermoscopic characteristics of nodular squamous cell carcinoma and keratoacanthoma.

BACKGROUND: Nodular squamous cell carcinoma (SCC) and keratoacanthoma (KA) may mimic a variety of other benign and malignant non-pigmented nodules. OBJECTIVES: To analyze the dermoscopic characteristics of nodular SCC and KA. PATIENTS/METHODS: Retrospective analysis of 50 nodular SCCs and 8 KAs collected from a tertiary dermatology referral center and a private dermatology practice in Melbourne, Australia, between 1 September 2009 and 1 October 2012. All lesions were nodules; defined as firm, elevated, round, palpable tumors with a diameter of 5 mm or more. Clinical and dermoscopic images were evaluated by two examiners in consensus. RESULTS: Signs of keratinization were frequently observed and included keratin crust/scale (90% of SCCs, 100% of KAs), central keratin mass (32% of SCCs, 88% of KAs), white structureless areas (66% of SCCs, 50% of KAs), white circles (32% of SCCs, 38% of KAs) and white keratin pearls (14% of SCCs, 12% of KAs). Hemorrhage was present in 72% of SCCs and 88% of KAs and preferentially occurred centrally and in areas of keratinization. For nodular SCCs and KAs, we observed glomerular vessels (42% and 25% respectively), linear irregular vessels (36% and 25% respectively), atypical vessels (30% and 38% respectively) and hairpin vessels (30% and 25% respectively). CONCLUSIONS: Hemorrhage, keratinization and vascular features (glomerular, hairpin and linear irregular morphologies) are useful in diagnosing both nodular SCC and KA. Further research on the comparative dermoscopic characteristics of a range of amelanotic nodules is important in order to improve diagnosis of these clinically challenging tumors.

IgG4-related disease with cutaneous manifestations treated with rituximab: case report and literature review.

Immunoglobulin type gamma 4 (Ig)G4-related disease (IgG4-RD) is a relatively recently described clinical entity characterised by elevated levels of serum IgG4 and tissue infiltration of IgG4+ plasma cells in various organ systems. Cutaneous involvement is rare but is becoming increasingly appreciated; typically presenting as erythematous papules and/or nodules that are commonly pruritic. We report a case of IgG4-RD presenting with persistent pruritic papules and unilateral parotid swelling. His serum IgG4 level was elevated and a histological examination of his skin biopsies found a lymphoplasmacytic infiltration with an excess of IgG4+ non-clonal plasma cells. The patient was intolerant of oral prednisolone, however complete resolution of the cutaneous lesions was achieved with the anti-CD20 antibody, rituximab.

Redox potential and the response of cardiac ryanodine receptors to CLIC-2, a member of the glutathione S-transferase structural family.

The type 2 chloride intracellular channel, CLIC-2, is a member of the glutathione S-transferase structural family and a suppressor of cardiac ryanodine receptor (RyR2) Ca2+ channels located in the membrane of the sarcoplasmic reticulum (SR). Modulators of RyR2 activity can alter cardiac contraction. Since both CLIC-2 and RyR2 are modified by redox reactions, we speculated that the action of CLIC-2 on RyR2 may depend on redox potential. We used a GSH:GSSG buffer system to produce mild changes in redox potential to influence redox sensors in RyR2 and CLIC-2. RyR2 activity was modified only when both luminal and cytoplasmic solutions contained the GSH:GSSG buffer and the effects were reversed by removing the buffer from one of the solutions. Channel activity increased with an oxidizing redox potential and decreased when the potential was more reducing. Addition of cytoplasmic CLIC-2 inhibited RyR2 with oxidizing redox potentials, but activated RyR2 under reducing conditions. The results suggested that both RyR2 and CLIC-2 contain redox sensors. Since cardiac ischemia involves a destructive Ca2+ overload that is partly due to oxidation-induced increase in RyR2 activity, we speculate that the properties of CLIC-2 place it in an ideal position to limit ischemia-induced cellular damage in cardiac muscle.