[A woman with hyperkeratotic papules on arms and legs]. / Een vrouw met witte verhardingen op armen en benen.

A 50-year old woman with hyperkeratotic verrucous papules and plaques visited the outpatient clinic of Dermatology. Histopathology showed hyperplasia of verrucous epithelia, orthokeratosis and an infiltrate, leading to the diagnosis 'verrucous (hypertrophic) lichen planus'. This skin condition is often misdiagnosed as psoriasis. Squamous cell carcinoma can develop within skin lesions.

High prevalence of autoimmune thyroiditis in children and adolescents with vitiligo.

BACKGROUND/AIMS: Vitiligo is considered to be an autoimmune disease and is known to be associated with other autoimmune diseases, particularly affecting the thyroid. In children and adolescents this association has been reported in only a few studies, with varying results. The aim of this study was to examine thyroid function and prevalence of thyroid autoimmunity in children and adolescents with vitiligo and to investigate the utility of screening. METHODS: Two hundred and sixty patients with vitiligo were enrolled. Plasma TSH, FT4 and anti-thyroid peroxidase (TPO) antibody concentrations were measured. The prevalence of thyroid dysfunction and autoimmunity were compared to the general healthy paediatric population. RESULTS: Autoimmune thyroiditis (AIT) with thyroid hormone disturbances was diagnosed in 16 patients (6.2%). This is significantly higher than the prevalence reported in the general healthy paediatric population. Increased levels of anti-TPO antibodies (= 30 kU/l), without thyroid hormone disturbances, were found in 27 patients (10.5%). CONCLUSION: The prevalence of AIT in children and adolescents with vitiligo is significantly higher than in the general population. It may be advantageous to screen thyroid function and antibody levels in all paediatric patients with non-segmental vitiligo. To strengthen recommendations on screening, research on the burden for patients and cost-effectiveness is needed.

Oncogene-induced cellular senescence.

Oncogene-induced senescence (OIS) is a robust and sustained antiproliferative response brought about by oncogenic signaling resulting from an activating mutation of an oncogene, or the inactivation of a tumor-suppressor gene. The pathways mediating OIS are complex and incompletely elucidated but, the proliferative arrest involves activation of both the RB and p53 pathways. In addition, whereas there are indications that at least in some situations, negative feedback loops abolish the increased mitogenic signaling resulting from the oncogenic mutations, also an unexpected contribution of interleukin-mediated signaling has recently been found. OIS brings about cessation of growth of some benign tumors, including melanocytic nevi and several other lesions, including pituitary and thyroid adenomas. It protects against progression to cancer, and in this way complements oncogene-induced apoptosis. Perhaps, OIS has evolved as an alternative to apoptosis especially regarding long-lived cell types that are not replaceable in large numbers. Contrary to the earlier belief, OIS is not entirely irreversible, at least in some well documented in vitro systems. This means that its induction does not entirely eliminate the oncogenic threat resulting from the mutated cell. It also means that OIS, or related phenomena that may affect a proportion of the tumor cells of some cancers, may have an influence on responsiveness to cytotoxic cancer therapies, because OIS is associated with an antiapoptosis phenotype.