Cutaneous T cell lymphoma complicating severe atopic dermatitis. Is making a diagnosis the main challenge?

The association between severe long-term atopic dermatitis (AD) and the risk of skin lymphoma is still a matter of debate, since epidemiological studies have shown contradictory results. We report 2 cases of patients with a documented history of severe longstanding atopic disease, who had never been treated with topical or systemic calcineurin inhibitors, and who developed a cytotoxic cutaneous T cell lymphoma (CTCL). For these 2 patients, clinical manifestations preceded the diagnosis of CTCL. The diagnosis was based on histological findings and molecular analysis of the T cell receptor (TCR) clonality. These cases illustrate the difficulty in diagnosing CTCL in patients with severe AD and extensive inflammatory skin lesions. The transition between severe AD and CTCL is progressive; histological findings and molecular evidence of TCR clonality are detected after the clinical changes. These 2 cases lend further support to the hypothesis of an association between severe long-term AD and CTCL.

Photodistribution of blue-gray hyperpigmentation after amiodarone treatment: molecular characterization of amiodarone in the skin.

BACKGROUND: For decades, the photodistributed blue-gray skin hyperpigmentation observed after amiodarone therapy was presumably attributed to dermal lipofuscinosis. Using electron microscopy and high-performance liquid chromatography, we identified amiodarone deposits in the hyperpigmented skin sample from a patient treated with this antiarrhythmic agent. Our findings therefore indicate that the hypothesis relating the blue-gray hyperpigmentation to lipofuscin should be challenged. OBSERVATIONS: A 64-year-old man, skin phototype III, presented with asymptomatic skin hyperpigmentation that had been slowly developing on sun-exposed areas since April 2004. He had been taking amiodarone for 4 years (cumulative dose, 277 g). Electron microscopy did not show lipofuscin pigments in his skin. Conversely, abundant electron-dense membrane-bound granule deposits were observed in most of the dermal cells (fibroblasts, macrophages, pericytes, Schwann cells, and endothelial cells), especially in photoexposed skin. High-performance liquid chromatography confirmed that the skin deposits were composed of amiodarone. These results demonstrate that amiodarone hyperpigmentation is related to drug deposition on photoexposed skin. CONCLUSION: Amiodarone-related hyperpigmentation should be considered a skin storage disease that is secondary to drug deposition.

KBA.62: a useful marker for primary and metastatic melanomas.

We previously described a novel antimelanoma antibody, designated KBA.62. However, review of the literature showed that only a few studies have reported on this antibody. We report our experience in the diagnosis of melanoma using KBA.62 and its value in both primary and metastatic conditions. In addition to conventional melanomas, we included desmoplastic and spindle cell melanomas, whose diagnosis can be challenging. We also focus on identification of malignant cells in sentinel lymph node biopsies using KBA.62, by comparison with anti-S-100 protein and HMB-45 antibodies, because discrepancies in sensitivity and specificity of melanoma markers have given rise to numerous studies aiming to determine the best panel for the evaluation of sentinel lymph node from patients with melanoma. Overall, KBA.62 was positive in 93% of primary and metastatic melanomas. Interestingly, the 12 cases of desmoplastic and spindle cell melanomas had strongly positive results. In addition, the results of our study performed on a series of 215 sentinel lymph nodes showed that the sensitivity of anti-S-100 protein and KBA.62 antibodies in detecting occult metastasis was similar. Moreover, KBA.62 identified 6 patients (3%) who had confirmed sentinel lymph node metastasis but were negative for HMB-45. The resolution was higher with KBA.62 than that observed with anti-S-100 protein antibody, as the nonmelanocytic positive cells for KBA.62 in lymph nodes were only represented by endothelial cells, which therefore constituted an intrinsic positive control. We conclude that KBA.62 antibody is a useful additional marker for melanoma, specifically in desmoplastic/spindle cell cases and in the context of micrometastasis in sentinel lymph node.