Women live one-third of their lives in the post-menopausal state. Significant hormonal alterations occur at the time of menopause, leading to a range of physiological disorders affecting multiple organ systems in the body. The effects of menopause on the skin have been underresearched. Many skin changes occur at the time of menopause and the cutaneous effects of hormone replacement therapy are significant. Menopausal changes in hormones may alter the biomechanical properties of the skin and certain disorders are more common in menopausal women, such as lichen sclerosus, atrophic vulvovaginitis, flushing and dysaesthetic vulvodynia. Hair and oral changes may also be associated. As the average life expectancy increases, dermatologists need to be familiar with skin diseases affecting women in this age group.

PC-1 is a useful antibody in a diagnostic immunohistochemical panel when investigating AFX and AFX-like tumors; however, good technical quality and careful interpretation are necessary when using a panel of antibodies, particularly to keratin and S-100 protein, for optimal accuracy.

This paper reviews the theories of the pathogenesis of atopic dermatitis (AD), with a particular emphasis on its immunopathogenesis. The contribution of predisposing factors, immunopathogenic factors and provoking factors in the pathogenesis of AD are considered. Predisposing factors explored in this article include genetics and the disturbance of skin function. Immunopathogenic factors reviewed include T cell dysfunction, biphasic cytokine expression and the role of immunoglobulin E. Provoking factors considered include microbial factors, psychosomatic interactions, contact allergens and irritants, inhalant allergens, food and climate. Immunosuppressive treatments reviewed include cyclosporin, azathioprine, methotrexate, tacrolimus, interferon-gamma, phosphodiesterase inhibitors and pimecrolimus (SDZ ASM 981).

Thalidomide is an effective agent to treat over 25 seemingly unrelated dermatological conditions that have an inflammatory or autoimmune basis. The main side-effects of teratogenesis and peripheral neuropathy limit its use. Currently, in Australia no assurance is given as to the quality, safety and efficacy of thalidomide. The use of thalidomide for toxic epidermal necrolysis can lead to an increase in mortality, and its use as a prophylactic agent for the prevention of chronic graft-versus-host disease following bone marrow transplantation has raised more speculations as to the safety of this notorious drug. A review of the therapeutic indications for thalidomide in dermatology as well as the mechanisms of action and side-effects of this drug are presented. The current suggested guidelines for its use in clinical practice in Australia are discussed.

Background The pathogenesis of delayed onset tissue nodules (DTNs) due to hyaluronic acid (HA) injections is uncertain. Objectives To formulate a rational theory for DTN development and their avoidance and treatment. Methods A multi-disciplinary and multi country DTN consensus panel was established with 20 questions posed and consensus sought. Consensus was set at 75% agreement. Results Consensus was reached in 16/20 questions regarding the pathogenesis of DTNs forming the basis of a classification and treatment guide. Conclusions The group believe that filler, pathogens and inflammation are all involved in DTNs and that DTNs most likely are infection initiated with a variable immune response. Injected filler may incorporate surface bacteria, either a commensal or a true pathogen if the skin barrier is altered. The initially High molecular weight HA (HMWHA) filler is degraded to Low molecular weight HA (LMWHA) at the edge of the filler. Commensals positioned within the filler bolus may be well tolerated until the filler is degraded and the commensal becomes visible to the immune system. LMWHA is particularly inflammatory in the presence of any local bacteria. Commensals may still be tolerated unless the immune system is generally heightened by viraemia, or vaccination. Systemic pathogenic bacteraemia may also interact with the filler peripheral LMWHA, activating Toll Like receptors inducing DTN formation. Given this scenario, attention to practitioner and patient hygiene and early systemic infection treatment deserve attention. Classification and treatment systems were devised by considering each of the 3 factors of filler, inflammation, and infection separately.