Making Sense of Late Tissue Nodules Associated With Hyaluronic Acid Injections.

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 multidisciplinary and multicountry DTN consensus panel was established, with 20 questions posed and consensus sought. Consensus was set at 75% agreement. RESULTS: Consensus was reached in 16 of 20 questions regarding the pathogenesis of DTNs, forming the basis for a classification and treatment guide. CONCLUSIONS: The group believes 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 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 viremia or vaccination. Systemic pathogenic bacteremia may also interact with the filler peripheral LMWHA, activating Toll-like receptors that induce 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-filler, inflammation, and infection-separately.

Strategies required to improve the management of chronic vulvar discomfort in Australia.

OBJECTIVE: To investigate factors required to improve the management of vulvar pain from a patient perspective. SAMPLE AND SETTING: Sixty patients in four different specialised vulvar clinics. METHODS: Women with chronic vulvar pain were asked to complete a questionnaire whilst waiting for specialist consultation by either a dermatologist, sexual health physican, psychologist or physiotherapist. RESULTS: The average length of time patients had vulvar pain was 6.03 years, with a mean of 5.83 practitioners seen. Twenty-seven per cent indicated that increased awareness of vulvodynia was required by gynaecologists and 74% suggested that increased general practitioner awareness was necessary to improve care. Accurate diagnosis, and understanding lifestyle implications were key elements of patient satisfaction, considered more important than any available treatment modality. CONCLUSIONS: Current services and skilled practitioners available for the management of chronic vulvar pain or vulvodynia in Australia do not reflect the estimated prevalence of this condition. From this study it was concluded that the three most important factors required to improve quality of care in order of importance were increased practitioner awareness, research and the setting up of more specialised multi-disciplinary clinics.

Thalidomide in dermatology.

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.

Atopic dermatitis: review of immunopathogenesis and advances in immunosuppressive therapy.

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).

Procollagen 1 expression in atypical fibroxanthoma and other tumors.

BACKGROUND: Procollagen (PC) is secreted by fibroblasts into the extracellular matrix, where it is cleaved to form collagen. The rat anti-human PC-1 monoclonal antibody has been reported to react with atypical fibroxanthoma (AFX), a poorly differentiated but usually benign skin lesion common in elderly patients. We have studied PC-1 staining in 50 tumors with AFX histological features (four of which were subsequently reclassified as non-AFX tumors) to confirm this prior observation. In addition, we have investigated PC-1 in other skin tumors, particularly those with spindled cell or sclerosing/desmoplastic morphologies. METHOD: Archival material was retrieved and sections were prepared and immunostained with PC-1 as well as a panel of antibodies, including S-100 and MNF-116 (cytokeratins 5, 6, 7, 8, 17, and 19). RESULTS: PC-1 staining was strongly positive in 40 of 46 (87%) AFXs. Three AFXs displayed weak staining with PC-1 even after repeat staining of 10 tumors that were initially weak. Three additional tumors stained with both PC-1 and MNF-116 and were classified as AFX-like squamous cell carcinoma (SCC). One tumor with AFX-like histology was PC-1 negative and S-100 positive and was classified as an AFX-like melanoma. Positive staining in tumor cells was observed in three of nine (33%) desmoplastic malignant melanomas, three of eight (38%) desmoplastic SCCs, zero of 10 (0%) desmoplastic trichoepitheliomas, zero of 10 (0%) morpheic basal cell carcinomas, and zero of 10 (0%) sclerosing sweat duct carcinomas. CONCLUSION: 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.